%% Papers Published
@article{fds374536,
Author = {Zavaliev, R and Dong, X},
Title = {NPR1, a key immune regulator for plant survival under biotic
and abiotic stresses.},
Journal = {Molecular cell},
Volume = {84},
Number = {1},
Pages = {131-141},
Year = {2024},
Month = {January},
url = {http://dx.doi.org/10.1016/j.molcel.2023.11.018},
Abstract = {Nonexpressor of pathogenesis-related genes 1 (NPR1) was
discovered in Arabidopsis as an activator of salicylic acid
(SA)-mediated immune responses nearly 30 years ago. How NPR1
confers resistance against a variety of pathogens and
stresses has been extensively studied; however, only in
recent years have the underlying molecular mechanisms been
uncovered, particularly NPR1's role in SA-mediated
transcriptional reprogramming, stress protein homeostasis,
and cell survival. Structural analyses ultimately defined
NPR1 and its paralogs as SA receptors. The SA-bound NPR1
dimer induces transcription by bridging two TGA
transcription factor dimers, forming an enhanceosome.
Moreover, NPR1 orchestrates its multiple functions through
the formation of distinct nuclear and cytoplasmic
biomolecular condensates. Furthermore, NPR1 plays a central
role in plant health by regulating the crosstalk between SA
and other defense and growth hormones. In this review, we
focus on these recent advances and discuss how NPR1 can be
utilized to engineer resistance against biotic and abiotic
stresses.},
Doi = {10.1016/j.molcel.2023.11.018},
Key = {fds374536}
}
@article{fds375251,
Author = {Spoel, SH and Dong, X},
Title = {Salicylic Acid in Plant Immunity and Beyond.},
Journal = {The Plant cell},
Pages = {koad329},
Year = {2024},
Month = {January},
url = {http://dx.doi.org/10.1093/plcell/koad329},
Abstract = {As the most widely used herbal medicine in human history and
a major defense hormone in plants against a broad spectrum
of pathogens and abiotic stresses, salicylic acid (SA) has
attracted major research interest. With applications of
modern technologies over the past 30 years, studies of the
effects of SA on plant growth, development, and defense have
revealed many new research frontiers, and continue to
deliver surprises. In this review, we provide an update on
recent advances in our understanding of SA metabolism,
perception, and signal transduction mechanisms in plant
immunity. An overarching theme emerges that SA executes its
many functions through intricate regulation at multiple
steps: SA biosynthesis is regulated both locally and
systemically, while its perception occurs through multiple
cellular targets, including metabolic enzymes, redox
regulators, transcription cofactors, and most recently, an
RNA-binding protein. Moreover, SA orchestrates a complex
series of posttranslational modifications of downstream
signaling components and promotes the formation of
biomolecular condensates that function as cellular signaling
hubs. SA also impacts wider cellular functions through
crosstalk with other plant hormones. Looking into the
future, we propose new areas for exploration on SA
functions, which will undoubtedly uncover more surprises for
many years to come.},
Doi = {10.1093/plcell/koad329},
Key = {fds375251}
}
@article{fds372647,
Author = {Xiang, Y and Huang, W and Tan, L and Chen, T and He, Y and Irving, PS and Weeks, KM and Zhang, QC and Dong, X},
Title = {Pervasive downstream RNA hairpins dynamically dictate
start-codon selection.},
Journal = {Nature},
Volume = {621},
Number = {7978},
Pages = {423-430},
Year = {2023},
Month = {September},
url = {http://dx.doi.org/10.1038/s41586-023-06500-y},
Abstract = {Translational reprogramming allows organisms to adapt to
changing conditions. Upstream start codons (uAUGs), which
are prevalently present in mRNAs, have crucial roles in
regulating translation by providing alternative translation
start sites<sup>1-4</sup>. However, what determines this
selective initiation of translation between conditions
remains unclear. Here, by integrating transcriptome-wide
translational and structural analyses during
pattern-triggered immunity in Arabidopsis, we found that
transcripts with immune-induced translation are enriched
with upstream open reading frames (uORFs). Without
infection, these uORFs are selectively translated owing to
hairpins immediately downstream of uAUGs, presumably by
slowing and engaging the scanning preinitiation complex.
Modelling using deep learning provides unbiased support for
these recognizable double-stranded RNA structures downstream
of uAUGs (which we term uAUG-ds) being responsible for the
selective translation of uAUGs, and allows the prediction
and rational design of translating uAUG-ds. We found that
uAUG-ds-mediated regulation can be generalized to human
cells. Moreover, uAUG-ds-mediated start-codon selection is
dynamically regulated. After immune challenge in plants,
induced RNA helicases that are homologous to Ded1p in yeast
and DDX3X in humans resolve these structures, allowing
ribosomes to bypass uAUGs to translate downstream defence
proteins. This study shows that mRNA structures dynamically
regulate start-codon selection. The prevalence of this RNA
structural feature and the conservation of RNA helicases
across kingdoms suggest that mRNA structural remodelling is
a general feature of translational reprogramming.},
Doi = {10.1038/s41586-023-06500-y},
Key = {fds372647}
}
@article{fds374934,
Author = {Cao, L and Yoo, H and Chen, T and Mwimba, M and Zhang, X and Dong,
X},
Title = {H2O2 sulfenylates CHE linking local infection to
establishment of systemic acquired resistance.},
Journal = {bioRxiv},
Year = {2023},
Month = {August},
url = {http://dx.doi.org/10.1101/2023.07.27.550865},
Abstract = {In plants, a local infection can lead to systemic acquired
resistance (SAR) through increased production of salicylic
acid (SA). For 30 years, the identity of the mobile signal
and its direct transduction mechanism for systemic SA
synthesis in initiating SAR have been hotly debated. We
found that, upon pathogen challenge, the cysteine residue of
transcription factor CHE undergoes sulfenylation in systemic
tissues, enhancing its binding to the promoter of
SA-synthesis gene, ICS1, and increasing SA production. This
occurs independently of previously reported pipecolic acid
(Pip) signal. Instead, H2O2 produced by NADPH oxidase,
RBOHD, is the mobile signal that sulfenylates CHE in a
concentration-dependent manner. This modification serves as
a molecular switch that activates CHE-mediated SA-increase
and subsequent Pip-accumulation in systemic tissues to
synergistically induce SAR.},
Doi = {10.1101/2023.07.27.550865},
Key = {fds374934}
}
@article{fds369931,
Author = {Zhou, P and Zavaliev, R and Xiang, Y and Dong, X},
Title = {Seeing is believing: Understanding functions of NPR1 and its
paralogs in plant immunity through cellular and structural
analyses.},
Journal = {Curr Opin Plant Biol},
Volume = {73},
Pages = {102352},
Year = {2023},
Month = {June},
url = {http://dx.doi.org/10.1016/j.pbi.2023.102352},
Abstract = {In the past 30 years, our knowledge of how nonexpressor of
pathogenesis-related genes 1 (NPR1) serves as a master
regulator of salicylic acid (SA)-mediated immune responses
in plants has been informed largely by molecular genetic
studies. Despite extensive efforts, the biochemical
functions of this protein in promoting plant survival
against a wide range of pathogens and abiotic stresses are
not completely understood. Recent breakthroughs in cellular
and structural analyses of NPR1 and its paralogs have
provided a molecular framework for reinterpreting decades of
genetic observations and have revealed new functions of
these proteins. Besides NPR1's well-known nuclear activity
in inducing stress-responsive genes, it has also been shown
to control stress protein homeostasis in the cytoplasm.
Structurally, NPR4's direct binding to SA has been
visualized at the molecular level. Analysis of the cryo-EM
and crystal structures of NPR1 reveals a bird-shaped
homodimer containing a unique zinc finger. Furthermore, the
TGA32-NPR12-TGA32 complex has been imaged, uncovering a
dimeric NPR1 bridging two TGA3 transcription factor dimers
as part of an enhanceosome complex to induce defense gene
expression. These new findings will shape future research
directions for deciphering NPR functions in plant
immunity.},
Doi = {10.1016/j.pbi.2023.102352},
Key = {fds369931}
}
@article{fds369671,
Author = {Chen, T and Xu, G and Mou, R and Greene, GH and Liu, L and Motley, J and Dong,
X},
Title = {Global translational induction during NLR-mediated immunity
in plants is dynamically regulated by CDC123, an
ATP-sensitive protein.},
Journal = {Cell host & microbe},
Volume = {31},
Number = {3},
Pages = {334-342.e5},
Year = {2023},
Month = {March},
url = {http://dx.doi.org/10.1016/j.chom.2023.01.014},
Abstract = {The recognition of pathogen effectors by their cognate
nucleotide-binding leucine-rich repeat (NLR) receptors
activates effector-triggered immunity (ETI) in plants. ETI
is associated with correlated transcriptional and
translational reprogramming and subsequent death of infected
cells. Whether ETI-associated translation is actively
regulated or passively driven by transcriptional dynamics
remains unknown. In a genetic screen using a translational
reporter, we identified CDC123, an ATP-grasp protein, as a
key activator of ETI-associated translation and defense.
During ETI, an increase in ATP concentration facilitates
CDC123-mediated assembly of the eukaryotic translation
initiation factor 2 (eIF2) complex. Because ATP is required
for the activation of NLRs as well as the CDC123 function,
we uncovered a possible mechanism by which the defense
translatome is coordinately induced during NLR-mediated
immunity. The conservation of the CDC123-mediated eIF2
assembly suggests its possible role in NLR-mediated immunity
beyond plants.},
Doi = {10.1016/j.chom.2023.01.014},
Key = {fds369671}
}
@article{fds365168,
Author = {Hua, J and Dong, X},
Title = {Sustaining plant immunity in rising temperature.},
Journal = {Cell research},
Volume = {32},
Number = {12},
Pages = {1038-1039},
Year = {2022},
Month = {December},
url = {http://dx.doi.org/10.1038/s41422-022-00710-1},
Doi = {10.1038/s41422-022-00710-1},
Key = {fds365168}
}
@article{fds365140,
Author = {Wang, J and Zhang, X and Greene, GH and Xu, G and Dong,
X},
Title = {PABP/purine-rich motif as an initiation module for
cap-independent translation in pattern-triggered
immunity.},
Journal = {Cell},
Volume = {185},
Number = {17},
Pages = {3186-3200.e17},
Year = {2022},
Month = {August},
url = {http://dx.doi.org/10.1016/j.cell.2022.06.037},
Abstract = {Upon stress, eukaryotes typically reprogram their
translatome through GCN2-mediated phosphorylation of the
eukaryotic translation initiation factor, eIF2α, to inhibit
general translation initiation while selectively translating
essential stress regulators. Unexpectedly, in plants,
pattern-triggered immunity (PTI) and response to other
environmental stresses occur independently of the
GCN2/eIF2α pathway. Here, we show that while PTI induces
mRNA decapping to inhibit general translation, defense mRNAs
with a purine-rich element ("R-motif") are selectively
translated using R-motif as an internal ribosome entry site
(IRES). R-motif-dependent translation is executed by
poly(A)-binding proteins (PABPs) through preferential
association with the PTI-activating eIFiso4G over the
repressive eIF4G. Phosphorylation by PTI regulators
mitogen-activated protein kinase 3 and 6 (MPK3/6) inhibits
eIF4G's activity while enhancing PABP binding to the R-motif
and promoting eIFiso4G-mediated defense mRNA translation,
establishing a link between PTI signaling and protein
synthesis. Given its prevalence in both plants and animals,
the PABP/R-motif translation initiation module may have a
broader role in reprogramming the stress
translatome.},
Doi = {10.1016/j.cell.2022.06.037},
Key = {fds365140}
}
@article{fds363217,
Author = {Kumar, S and Zavaliev, R and Wu, Q and Zhou, Y and Cheng, J and Dillard, L and Powers, J and Withers, J and Zhao, J and Guan, Z and Borgnia, MJ and Bartesaghi, A and Dong, X and Zhou, P},
Title = {Structural basis of NPR1 in activating plant
immunity.},
Journal = {Nature},
Volume = {605},
Number = {7910},
Pages = {561-566},
Year = {2022},
Month = {May},
url = {http://dx.doi.org/10.1038/s41586-022-04699-w},
Abstract = {NPR1 is a master regulator of the defence transcriptome
induced by the plant immune signal salicylic acid1-4.
Despite the important role of NPR1 in plant immunity5-7,
understanding of its regulatory mechanisms has been hindered
by a lack of structural information. Here we report
cryo-electron microscopy and crystal structures of
Arabidopsis NPR1 and its complex with the transcription
factor TGA3. Cryo-electron microscopy analysis reveals that
NPR1 is a bird-shaped homodimer comprising a central
Broad-complex, Tramtrack and Bric-à-brac (BTB) domain, a
BTB and carboxyterminal Kelch helix bundle, four ankyrin
repeats and a disordered salicylic-acid-binding domain.
Crystal structure analysis reveals a unique zinc-finger
motif in BTB for interacting with ankyrin repeats and
mediating NPR1 oligomerization. We found that, after
stimulation, salicylic-acid-induced folding and docking of
the salicylic-acid-binding domain onto ankyrin repeats is
required for the transcriptional cofactor activity of NPR1,
providing a structural explanation for a direct role of
salicylic acid in regulating NPR1-dependent gene expression.
Moreover, our structure of the TGA32-NPR12-TGA32 complex,
DNA-binding assay and genetic data show that dimeric NPR1
activates transcription by bridging two fatty-acid-bound
TGA3 dimers to form an enhanceosome. The stepwise assembly
of the NPR1-TGA complex suggests possible hetero-oligomeric
complex formation with other transcription factors,
revealing how NPR1 reprograms the defence
transcriptome.},
Doi = {10.1038/s41586-022-04699-w},
Key = {fds363217}
}
@article{fds362150,
Author = {Zhang, X and Dong, X},
Title = {Life-or-death decisions in plant immunity.},
Journal = {Current opinion in immunology},
Volume = {75},
Pages = {102169},
Year = {2022},
Month = {April},
url = {http://dx.doi.org/10.1016/j.coi.2022.102169},
Abstract = {Upon pathogen challenge, plant cells can mount defense not
only by triggering programmed cell death (PCD) to limit
pathogen growth, but also by secreting immune signals to
activate subsequent organism-scale defense responses. Recent
advances in the study of plant immune mechanisms have found
that pathogen-induced oligomerization of immune receptors is
a common 'on' switch for the normally self-inhibitory
proteins. The resulting 'resistosome' triggers PCD through
the formation of a calcium channel or a NADase. Synergy
between different receptor-mediated signaling pathways
appears to be required for sustained immune induction to
trigger PCD of infected cells. In the neighboring cells, PCD
is inhibited through the production of immune signal
salicylic acid (SA) which mediates degradation of
PCD-inducing immune components in biomolecular condensates.
Future work is required to connect the resistosome-mediated
channel formation and the NADase activity to the downstream
regulation of immune execution.},
Doi = {10.1016/j.coi.2022.102169},
Key = {fds362150}
}
@article{fds355679,
Author = {McMillan, HM and Zebell, SG and Ristaino, JB and Dong, X and Kuehn,
MJ},
Title = {Protective plant immune responses are elicited by bacterial
outer membrane vesicles.},
Journal = {Cell Rep},
Volume = {34},
Number = {3},
Pages = {108645},
Year = {2021},
Month = {January},
url = {http://dx.doi.org/10.1016/j.celrep.2020.108645},
Abstract = {Bacterial outer membrane vesicles (OMVs) perform a variety
of functions in bacterial survival and virulence. In
mammalian systems, OMVs activate immune responses and are
exploited as vaccines. However, little work has focused on
the interactions of OMVs with plant hosts. Here, we report
that OMVs from Pseudomonas syringae and P. fluorescens
activate plant immune responses that protect against
bacterial and oomycete pathogens. OMV-mediated
immunomodulatory activity from these species displayed
different sensitivity to biochemical stressors, reflecting
differences in OMV content. Importantly, OMV-mediated plant
responses are distinct from those triggered by conserved
bacterial epitopes or effector molecules alone. Our study
shows that OMV-induced protective immune responses are
independent of the T3SS and protein, but that OMV-mediated
seedling growth inhibition largely depends on proteinaceous
components. OMVs provide a unique opportunity to understand
the interplay between virulence and host response strategies
and add a new dimension to consider in host-microbe
interactions.},
Doi = {10.1016/j.celrep.2020.108645},
Key = {fds355679}
}
@article{fds351421,
Author = {Wang, W and Withers, J and Li, H and Zwack, PJ and Rusnac, D-V and Shi, H and Liu, L and Yan, S and Hinds, TR and Guttman, M and Dong, X and Zheng,
N},
Title = {Structural basis of salicylic acid perception by Arabidopsis
NPR proteins.},
Journal = {Nature},
Volume = {586},
Number = {7828},
Pages = {311-316},
Year = {2020},
Month = {October},
url = {http://dx.doi.org/10.1038/s41586-020-2596-y},
Abstract = {Salicylic acid (SA) is a plant hormone that is critical for
resistance to pathogens<sup>1-3</sup>. The NPR proteins have
previously been identified as SA receptors<sup>4-10</sup>,
although how they perceive SA and coordinate hormonal
signalling remain unknown. Here we report the mapping of the
SA-binding core of Arabidopsis thaliana NPR4 and its
ligand-bound crystal structure. The SA-binding core domain
of NPR4 refolded with SA adopts an α-helical fold that
completely buries SA in its hydrophobic core. The lack of a
ligand-entry pathway suggests that SA binding involves a
major conformational remodelling of the SA-binding core of
NPR4, which we validated using hydrogen-deuterium-exchange
mass spectrometry analysis of the full-length protein and
through SA-induced disruption of interactions between NPR1
and NPR4. We show that, despite the two proteins sharing
nearly identical hormone-binding residues, NPR1 displays
minimal SA-binding activity compared to NPR4. We further
identify two surface residues of the SA-binding core, the
mutation of which can alter the SA-binding ability of NPR4
and its interaction with NPR1. We also demonstrate that
expressing a variant of NPR4 that is hypersensitive to SA
could enhance SA-mediated basal immunity without
compromising effector-triggered immunity, because the
ability of this variant to re-associate with NPR1 at high
levels of SA remains intact. By revealing the structural
mechanisms of SA perception by NPR proteins, our work paves
the way for future investigation of the specific roles of
these proteins in SA signalling and their potential for
engineering plant immunity.},
Doi = {10.1038/s41586-020-2596-y},
Key = {fds351421}
}
@article{fds352371,
Author = {Zhang, J and Coaker, G and Zhou, J-M and Dong, X},
Title = {Plant Immune Mechanisms: From Reductionistic to Holistic
Points of View.},
Journal = {Molecular plant},
Volume = {13},
Number = {10},
Pages = {1358-1378},
Year = {2020},
Month = {October},
url = {http://dx.doi.org/10.1016/j.molp.2020.09.007},
Abstract = {After three decades of the amazing progress made on
molecular studies of plant-microbe interactions (MPMI), we
have begun to ask ourselves "what are the major questions
still remaining?" as if the puzzle has only a few pieces
missing. Such an exercise has ultimately led to the
realization that we still have many more questions than
answers. Therefore, it would be an impossible task for us to
project a coherent "big picture" of the MPMI field in a
single review. Instead, we provide our opinions on where we
would like to go in our research as an invitation to the
community to join us in this exploration of new MPMI
frontiers.},
Doi = {10.1016/j.molp.2020.09.007},
Key = {fds352371}
}
@article{fds351422,
Author = {Zavaliev, R and Mohan, R and Chen, T and Dong, X},
Title = {Formation of NPR1 Condensates Promotes Cell Survival during
the Plant Immune Response.},
Journal = {Cell},
Volume = {182},
Number = {5},
Pages = {1093-1108.e18},
Year = {2020},
Month = {September},
url = {http://dx.doi.org/10.1016/j.cell.2020.07.016},
Abstract = {In plants, pathogen effector-triggered immunity (ETI) often
leads to programmed cell death, which is restricted by NPR1,
an activator of systemic acquired resistance. However, the
biochemical activities of NPR1 enabling it to promote
defense and restrict cell death remain unclear. Here we show
that NPR1 promotes cell survival by targeting substrates for
ubiquitination and degradation through formation of
salicylic acid-induced NPR1 condensates (SINCs). SINCs are
enriched with stress response proteins, including
nucleotide-binding leucine-rich repeat immune receptors,
oxidative and DNA damage response proteins, and protein
quality control machineries. Transition of NPR1 into
condensates is required for formation of the NPR1-Cullin 3
E3 ligase complex to ubiquitinate SINC-localized substrates,
such as EDS1 and specific WRKY transcription factors, and
promote cell survival during ETI. Our analysis of SINCs
suggests that NPR1 is centrally integrated into the cell
death or survival decisions in plant immunity by modulating
multiple stress-responsive processes in this
quasi-organelle.},
Doi = {10.1016/j.cell.2020.07.016},
Key = {fds351422}
}
@article{fds346565,
Author = {Yoo, H and Greene, GH and Yuan, M and Xu, G and Burton, D and Liu, L and Marqués, J and Dong, X},
Title = {Translational Regulation of Metabolic Dynamics during
Effector-Triggered Immunity.},
Journal = {Molecular plant},
Volume = {13},
Number = {1},
Pages = {88-98},
Year = {2020},
Month = {January},
url = {http://dx.doi.org/10.1016/j.molp.2019.09.009},
Abstract = {Recent studies have shown that global translational
reprogramming is an early activation event in
pattern-triggered immunity, when plants recognize
microbe-associated molecular patterns. However, it is not
fully known whether translational regulation also occurs in
subsequent immune responses, such as effector-triggered
immunity (ETI). In this study, we performed genome-wide
ribosome profiling in Arabidopsis upon RPS2-mediated ETI
activation and discovered that specific groups of genes were
translationally regulated, mostly in coordination with
transcription. These genes encode enzymes involved in
aromatic amino acid, phenylpropanoid, camalexin, and
sphingolipid metabolism. The functional significance of
these components in ETI was confirmed by genetic and
biochemical analyses. Our findings provide new insights into
diverse translational regulation of plant immune responses
and demonstrate that translational coordination of metabolic
gene expression is an important strategy for
ETI.},
Doi = {10.1016/j.molp.2019.09.009},
Key = {fds346565}
}
@article{fds346834,
Author = {Li, M and Cao, L and Mwimba, M and Zhou, Y and Li, L and Zhou, M and Schnable,
PS and O'Rourke, JA and Dong, X and Wang, W},
Title = {Comprehensive mapping of abiotic stress inputs into the
soybean circadian clock.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {116},
Number = {47},
Pages = {23840-23849},
Year = {2019},
Month = {November},
url = {http://dx.doi.org/10.1073/pnas.1708508116},
Abstract = {The plant circadian clock evolved to increase fitness by
synchronizing physiological processes with environmental
oscillations. Crop fitness was artificially selected through
domestication and breeding, and the circadian clock was
identified by both natural and artificial selections as a
key to improved fitness. Despite progress in
<i>Arabidopsis</i>, our understanding of the crop circadian
clock is still limited, impeding its rational improvement
for enhanced fitness. To unveil the interactions between the
crop circadian clock and various environmental cues, we
comprehensively mapped abiotic stress inputs to the soybean
circadian clock using a 2-module discovery pipeline. Using
the "molecular timetable" method, we computationally
surveyed publicly available abiotic stress-related soybean
transcriptomes to identify stresses that have strong impacts
on the global rhythm. These findings were then
experimentally confirmed using a multiplexed RNA sequencing
technology. Specific clock components modulated by each
stress were further identified. This comprehensive mapping
uncovered inputs to the plant circadian clock such as
alkaline stress. Moreover, short-term iron deficiency
targeted different clock components in soybean and
<i>Arabidopsis</i> and thus had opposite effects on the
clocks of these 2 species. Comparing soybean varieties with
different iron uptake efficiencies suggests that phase
modulation might be a mechanism to alleviate iron deficiency
symptoms in soybean. These unique responses in soybean
demonstrate the need to directly study crop circadian
clocks. Our discovery pipeline may serve as a broadly
applicable tool to facilitate these explorations.},
Doi = {10.1073/pnas.1708508116},
Key = {fds346834}
}
@article{fds350986,
Author = {Mcmillan, HM and Zebell, SG and Dong, X and Kuehn,
MJ},
Title = {Bacterial vesicles: Double agents for plant
defense},
Journal = {MOLECULAR PLANT-MICROBE INTERACTIONS},
Volume = {32},
Number = {10},
Pages = {34-35},
Publisher = {AMER PHYTOPATHOLOGICAL SOC},
Year = {2019},
Month = {October},
Key = {fds350986}
}
@article{fds355680,
Author = {Mwimba, M and Dong, X},
Title = {Quantification of the humidity effect on HR by Ion leakage
assay.},
Journal = {Bio-protocol},
Volume = {9},
Number = {7},
Pages = {e3203},
Year = {2019},
Month = {April},
url = {http://dx.doi.org/10.21769/bioprotoc.3203},
Abstract = {We describe a protocol to measure the contribution of
humidity on cell death during the effector-triggered
immunity (ETI), the plant immune response triggered by the
recognition of pathogen effectors by plant resistance genes.
This protocol quantifies tissue cell death by measuring ion
leakage due to loss of membrane integrity during the
hypersensitive response (HR), the ETI-associated cell death.
The method is simple and short enough to handle many
biological replicates, which improves the power of test of
statistical significance. The protocol is easily applicable
to other environmental cues, such as light and temperature,
or treatment with chemicals.},
Doi = {10.21769/bioprotoc.3203},
Key = {fds355680}
}
@article{fds339222,
Author = {Mwimba, M and Karapetyan, S and Liu, L and Marqués, J and McGinnis, EM and Buchler, NE and Dong, X},
Title = {Daily humidity oscillation regulates the circadian clock to
influence plant physiology.},
Journal = {Nature communications},
Volume = {9},
Number = {1},
Pages = {4290},
Year = {2018},
Month = {October},
url = {http://dx.doi.org/10.1038/s41467-018-06692-2},
Abstract = {Early circadian studies in plants by de Mairan and de
Candolle alluded to a regulation of circadian clocks by
humidity. However, this regulation has not been described in
detail, nor has its influence on physiology
been demonstrated. Here we report that, under constant
light, circadian humidity oscillation can entrain the plant
circadian clock to a period of 24 h probably through the
induction of clock genes such as CIRCADIAN CLOCK ASSOCIATED
1. Under simulated natural light and humidity cycles,
humidity oscillation increases the amplitude of the
circadian clock and further improves plant fitness-related
traits. In addition, humidity oscillation enhances
effector-triggered immunity at night possibly to counter
increased pathogen virulence under high humidity. These
results indicate that the humidity oscillation regulates
specific circadian outputs besides those co-regulated with
the light-dark cycle.},
Doi = {10.1038/s41467-018-06692-2},
Key = {fds339222}
}
@article{fds337576,
Author = {Greene, GH and Dong, X},
Title = {To grow and to defend.},
Journal = {Science (New York, N.Y.)},
Volume = {361},
Number = {6406},
Pages = {976-977},
Year = {2018},
Month = {September},
url = {http://dx.doi.org/10.1126/science.aau9065},
Doi = {10.1126/science.aau9065},
Key = {fds337576}
}
@article{fds331226,
Author = {Karapetyan, S and Dong, X},
Title = {Redox and the circadian clock in plant immunity: A balancing
act.},
Journal = {Free radical biology & medicine},
Volume = {119},
Pages = {56-61},
Year = {2018},
Month = {May},
url = {http://dx.doi.org/10.1016/j.freeradbiomed.2017.12.024},
Abstract = {Plants' reliance on sunlight for energy makes their
light-driven circadian clock a critical regulator in
balancing the energy needs for vital activities such as
growth and defense. Recent studies show that the circadian
clock acts as a strategic planner to prime active defense
responses towards the morning or daytime when conditions,
such as the opening of stomata required for photosynthesis,
are favorable for attackers. Execution of the defense
response, on the other hand, is determined according to the
cellular redox state and is regulated in part by the
production of reactive oxygen and nitrogen species upon
pathogen challenge. The interplay between redox and the
circadian clock further gates the onset of defense response
to a specific time of the day to avoid conflict with
growth-related activities. In this review, we focus on
discussing the roles of the circadian clock as a robust
overseer and the cellular redox as a dynamic executor of
plant defense.},
Doi = {10.1016/j.freeradbiomed.2017.12.024},
Key = {fds331226}
}
@article{fds327320,
Author = {Gu, Y and Zavaliev, R and Dong, X},
Title = {Membrane Trafficking in Plant Immunity.},
Journal = {Molecular plant},
Volume = {10},
Number = {8},
Pages = {1026-1034},
Year = {2017},
Month = {August},
url = {http://dx.doi.org/10.1016/j.molp.2017.07.001},
Abstract = {Plants employ sophisticated mechanisms to interact with
pathogenic as well as beneficial microbes. Of those,
membrane trafficking is key in establishing a rapid and
precise response. Upon interaction with pathogenic microbes,
surface-localized immune receptors undergo endocytosis for
signal transduction and activity regulation while cell wall
components, antimicrobial compounds, and defense proteins
are delivered to pathogen invasion sites through polarized
secretion. To sustain mutualistic associations, host cells
also reprogram the membrane trafficking system to
accommodate invasive structures of symbiotic microbes. Here,
we provide an analysis of recent advances in understanding
the roles of secretory and endocytic membrane trafficking
pathways in plant immune activation. We also discuss
strategies deployed by adapted microbes to manipulate these
pathways to subvert or inhibit plant defense.},
Doi = {10.1016/j.molp.2017.07.001},
Key = {fds327320}
}
@article{fds327321,
Author = {Withers, J and Dong, X},
Title = {Post-translational regulation of plant immunity.},
Journal = {Current opinion in plant biology},
Volume = {38},
Pages = {124-132},
Year = {2017},
Month = {August},
url = {http://dx.doi.org/10.1016/j.pbi.2017.05.004},
Abstract = {Plants have evolved multi-layered molecular defense
strategies to protect against pathogens. Plant immune
signaling largely relies on post-translational modifications
(PTMs) to induce rapid alterations of signaling pathways to
achieve a response that is appropriate to the type of
pathogen and infection pressure. In host cells, dynamic PTMs
have emerged as powerful regulatory mechanisms that cells
use to adjust their immune response. PTM is also a virulence
strategy used by pathogens to subvert host immunity through
the activities of effector proteins secreted into the host
cell. Recent studies focusing on deciphering
post-translational mechanisms underlying plant immunity have
offered an in-depth view of how PTMs facilitate efficient
immune responses and have provided a more dynamic and
holistic view of plant immunity.},
Doi = {10.1016/j.pbi.2017.05.004},
Key = {fds327321}
}
@article{fds326477,
Author = {Xu, G and Yuan, M and Ai, C and Liu, L and Zhuang, E and Karapetyan, S and Wang, S and Dong, X},
Title = {uORF-mediated translation allows engineered plant disease
resistance without fitness costs.},
Journal = {Nature},
Volume = {545},
Number = {7655},
Pages = {491-494},
Year = {2017},
Month = {May},
url = {http://dx.doi.org/10.1038/nature22372},
Abstract = {Controlling plant disease has been a struggle for humankind
since the advent of agriculture. Studies of plant immune
mechanisms have led to strategies of engineering resistant
crops through ectopic transcription of plants' own defence
genes, such as the master immune regulatory gene NPR1 (ref.
1). However, enhanced resistance obtained through such
strategies is often associated with substantial penalties to
fitness, making the resulting products undesirable for
agricultural applications. To remedy this problem, we sought
more stringent mechanisms of expressing defence proteins. On
the basis of our latest finding that translation of key
immune regulators, such as TBF1 (ref. 3), is rapidly and
transiently induced upon pathogen challenge (see
accompanying paper), we developed a 'TBF1-cassette'
consisting of not only the immune-inducible promoter but
also two pathogen-responsive upstream open reading frames
(uORFs<sub>TBF1</sub>) of the TBF1 gene. Here we demonstrate
that inclusion of uORFs<sub>TBF1</sub>-mediated
translational control over the production of snc1-1 (an
autoactivated immune receptor) in Arabidopsis thaliana and
AtNPR1 in rice enables us to engineer broad-spectrum disease
resistance without compromising plant fitness in the
laboratory or in the field. This broadly applicable strategy
may lead to decreased pesticide use and reduce the selective
pressure for resistant pathogens.},
Doi = {10.1038/nature22372},
Key = {fds326477}
}
@article{fds326478,
Author = {Xu, G and Greene, GH and Yoo, H and Liu, L and Marqués, J and Motley, J and Dong, X},
Title = {Global translational reprogramming is a fundamental layer of
immune regulation in plants.},
Journal = {Nature},
Volume = {545},
Number = {7655},
Pages = {487-490},
Year = {2017},
Month = {May},
url = {http://dx.doi.org/10.1038/nature22371},
Abstract = {In the absence of specialized immune cells, the need for
plants to reprogram transcription to transition from
growth-related activities to defence is well understood.
However, little is known about translational changes that
occur during immune induction. Using ribosome footprinting,
here we perform global translatome profiling on Arabidopsis
exposed to the microbe-associated molecular pattern elf18.
We find that during this pattern-triggered immunity,
translation is tightly regulated and poorly correlated with
transcription. Identification of genes with altered
translational efficiency leads to the discovery of novel
regulators of this immune response. Further investigation of
these genes shows that messenger RNA sequence features are
major determinants of the observed translational efficiency
changes. In the 5' leader sequences of transcripts with
increased translational efficiency, we find a highly
enriched messenger RNA consensus sequence, R-motif,
consisting of mostly purines. We show that R-motif regulates
translation in response to pattern-triggered immunity
induction through interaction with poly(A)-binding proteins.
Therefore, this study provides not only strong evidence, but
also a molecular mechanism, for global translational
reprogramming during pattern-triggered immunity in
plants.},
Doi = {10.1038/nature22371},
Key = {fds326478}
}
@article{fds324218,
Author = {Mwimba, M and Dong, X},
Title = {The CAT(2) Comes Back.},
Journal = {Cell host & microbe},
Volume = {21},
Number = {2},
Pages = {125-127},
Year = {2017},
Month = {February},
url = {http://dx.doi.org/10.1016/j.chom.2017.01.012},
Abstract = {Genetic and biochemical evidence supporting CATALASE2 as a
salicylic acid (SA) receptor has finally emerged. In this
issue of Cell Host & Microbe, Yuan et al. (2017) show that
SA binds to CATALASE2 to inhibit auxin and jasmonic acid
biosynthetic enzymes as a means to strengthen plant immunity
against biotrophic pathogens.},
Doi = {10.1016/j.chom.2017.01.012},
Key = {fds324218}
}
@article{fds322287,
Author = {Liu, L and Sonbol, F-M and Huot, B and Gu, Y and Withers, J and Mwimba, M and Yao, J and He, SY and Dong, X},
Title = {Salicylic acid receptors activate jasmonic acid signalling
through a non-canonical pathway to promote
effector-triggered immunity.},
Journal = {Nature communications},
Volume = {7},
Pages = {13099},
Year = {2016},
Month = {October},
url = {http://dx.doi.org/10.1038/ncomms13099},
Abstract = {It is an apparent conundrum how plants evolved
effector-triggered immunity (ETI), involving programmed cell
death (PCD), as a major defence mechanism against biotrophic
pathogens, because ETI-associated PCD could leave them
vulnerable to necrotrophic pathogens that thrive on dead
host cells. Interestingly, during ETI, the normally
antagonistic defence hormones, salicylic acid (SA) and
jasmonic acid (JA) associated with defence against biotrophs
and necrotrophs respectively, both accumulate to high
levels. In this study, we made the surprising finding that
JA is a positive regulator of RPS2-mediated ETI. Early
induction of JA-responsive genes and de novo JA synthesis
following SA accumulation is activated through the SA
receptors NPR3 and NPR4, instead of the JA receptor COI1. We
provide evidence that NPR3 and NPR4 may mediate this effect
by promoting degradation of the JA transcriptional repressor
JAZs. This unique interplay between SA and JA offers a
possible explanation of how plants can mount defence against
a biotrophic pathogen without becoming vulnerable to
necrotrophic pathogens.},
Doi = {10.1038/ncomms13099},
Key = {fds322287}
}
@article{fds325993,
Author = {Zavaliev, R and Dong, X and Epel, BL},
Title = {Glycosylphosphatidylinositol (GPI) Modification Serves as a
Primary Plasmodesmal Sorting Signal.},
Journal = {Plant physiology},
Volume = {172},
Number = {2},
Pages = {1061-1073},
Year = {2016},
Month = {October},
url = {http://dx.doi.org/10.1104/pp.16.01026},
Abstract = {Plasmodesmata (Pd) are membranous channels that serve as a
major conduit for cell-to-cell communication in plants. The
Pd-associated β-1,3-glucanase (BG_pap) and CALLOSE BINDING
PROTEIN1 (PDCB1) were identified as key regulators of Pd
conductivity. Both are predicted glycosylphosphatidylinositol-anchored
proteins (GPI-APs) carrying a conserved GPI modification
signal. However, the subcellular targeting mechanism of
these proteins is unknown, particularly in the context of
other GPI-APs not associated with Pd Here, we conducted a
comparative analysis of the subcellular targeting of the two
Pd-resident and two unrelated non-Pd GPI-APs in Arabidopsis
(Arabidopsis thaliana). We show that GPI modification is
necessary and sufficient for delivering both BG_pap and
PDCB1 to Pd Moreover, the GPI modification signal from both
Pd- and non-Pd GPI-APs is able to target a reporter protein
to Pd, likely to plasma membrane microdomains enriched at Pd
As such, the GPI modification serves as a primary Pd sorting
signal in plant cells. Interestingly, the ectodomain, a
region that carries the functional domain in GPI-APs, in
Pd-resident proteins further enhances Pd accumulation.
However, in non-Pd GPI-APs, the ectodomain overrides the Pd
targeting function of the GPI signal and determines a
specific GPI-dependent non-Pd localization of these proteins
at the plasma membrane and cell wall. Domain-swap analysis
showed that the non-Pd localization is also dominant over
the Pd-enhancing function mediated by a Pd ectodomain. In
conclusion, our results indicate that segregation between
Pd- and non-Pd GPI-APs occurs prior to Pd targeting,
providing, to our knowledge, the first evidence of the
mechanism of GPI-AP sorting in plants.},
Doi = {10.1104/pp.16.01026},
Key = {fds325993}
}
@article{fds322288,
Author = {Gu, Y and Zebell, SG and Liang, Z and Wang, S and Kang, B-H and Dong,
X},
Title = {Nuclear Pore Permeabilization Is a Convergent Signaling
Event in Effector-Triggered Immunity.},
Journal = {Cell},
Volume = {166},
Number = {6},
Pages = {1526-1538.e11},
Year = {2016},
Month = {September},
url = {http://dx.doi.org/10.1016/j.cell.2016.07.042},
Abstract = {Nuclear transport of immune receptors, signal transducers,
and transcription factors is an essential regulatory
mechanism for immune activation. Whether and how this
process is regulated at the level of the nuclear pore
complex (NPC) remains unclear. Here, we report that CPR5,
which plays a key inhibitory role in effector-triggered
immunity (ETI) and programmed cell death (PCD) in plants, is
a novel transmembrane nucleoporin. CPR5 associates with
anchors of the NPC selective barrier to constrain nuclear
access of signaling cargos and sequesters cyclin-dependent
kinase inhibitors (CKIs) involved in ETI signal
transduction. Upon activation by immunoreceptors, CPR5
undergoes an oligomer to monomer conformational switch,
which coordinates CKI release for ETI signaling and
reconfigures the selective barrier to allow significant
influx of nuclear signaling cargos through the NPC.
Consequently, these coordinated NPC actions result in
simultaneous activation of diverse stress-related signaling
pathways and constitute an essential regulatory mechanism
specific for ETI/PCD induction.},
Doi = {10.1016/j.cell.2016.07.042},
Key = {fds322288}
}
@article{fds322289,
Author = {Withers, J and Dong, X},
Title = {Posttranslational Modifications of NPR1: A Single Protein
Playing Multiple Roles in Plant Immunity and
Physiology.},
Journal = {PLoS pathogens},
Volume = {12},
Number = {8},
Pages = {e1005707},
Year = {2016},
Month = {August},
url = {http://dx.doi.org/10.1371/journal.ppat.1005707},
Doi = {10.1371/journal.ppat.1005707},
Key = {fds322289}
}
@article{fds322290,
Author = {Saleh, A and Withers, J and Mohan, R and Marqués, J and Gu, Y and Yan, S and Zavaliev, R and Nomoto, M and Tada, Y and Dong, X},
Title = {Erratum: Posttranslational Modifications of the Master
Transcriptional Regulator NPR1 Enable Dynamic but Tight
Control of Plant Immune Responses (Cell Host and Microbe
(2015) 18 (169-182))},
Journal = {Cell Host and Microbe},
Volume = {19},
Number = {1},
Pages = {127-130},
Publisher = {Elsevier BV},
Year = {2016},
Month = {January},
url = {http://dx.doi.org/10.1016/j.chom.2015.12.008},
Doi = {10.1016/j.chom.2015.12.008},
Key = {fds322290}
}
@article{fds290765,
Author = {Zebell, SG and Dong, X},
Title = {Cell-Cycle Regulators and Cell Death in Immunity.},
Journal = {Cell host & microbe},
Volume = {18},
Number = {4},
Pages = {402-407},
Year = {2015},
Month = {October},
ISSN = {1931-3128},
url = {http://dx.doi.org/10.1016/j.chom.2015.10.001},
Abstract = {Various cell death mechanisms are integral to host defense
in both plants and mammals. Plant defense against biotrophic
pathogens is associated with programmed cell death (PCD) of
the infected cell. This effector-triggered PCD is partly
analogous to pyroptosis, an inflammatory host cell death
process that plays a crucial role in defense against
microbial infections in mammals. Plant effector-triggered
PCD also shares with mammalian apoptosis the involvement of
cell-cycle regulators as signaling components. Here we
explore the similarities between these different cell death
programs as they relate to host defense and their
relationship to the cell cycle.},
Doi = {10.1016/j.chom.2015.10.001},
Key = {fds290765}
}
@article{fds228272,
Author = {Yang, L and Li, B and Zheng, XY and Li, J and Yang, M and Dong, X and He, G and An, C and Deng, XW},
Title = {Erratum: Salicylic acid biosynthesis is enhanced and
contributes to increased biotrophic pathogen resistance in
Arabidopsis hybrids (Nature Communications (2015) 6 (7309)
DOI: 10.1038/ncomms8309)},
Journal = {Nature Communications},
Volume = {6},
Number = {1},
Pages = {8145-8145},
Publisher = {Springer Nature},
Year = {2015},
Month = {August},
url = {http://dx.doi.org/10.1038/ncomms9145},
Doi = {10.1038/ncomms9145},
Key = {fds228272}
}
@article{fds322291,
Author = {Saleh, A and Withers, J and Mohan, R and Marqués, J and Gu, Y and Yan, S and Zavaliev, R and Nomoto, M and Tada, Y and Dong, X},
Title = {Posttranslational Modifications of the Master
Transcriptional Regulator NPR1 Enable Dynamic but Tight
Control of Plant Immune Responses.},
Journal = {Cell host & microbe},
Volume = {18},
Number = {2},
Pages = {169-182},
Year = {2015},
Month = {August},
url = {http://dx.doi.org/10.1016/j.chom.2015.07.005},
Abstract = {NPR1, a master regulator of basal and systemic acquired
resistance in plants, confers immunity through a
transcriptional cascade, which includes transcription
activators (e.g., TGA3) and repressors (e.g., WRKY70),
leading to the massive induction of antimicrobial genes. How
this single protein orchestrates genome-wide transcriptional
reprogramming in response to immune stimulus remains a major
question. Paradoxically, while NPR1 is essential for defense
gene induction, its turnover appears to be required for this
function, suggesting that NPR1 activity and degradation are
dynamically regulated. Here we show that sumoylation of NPR1
by SUMO3 activates defense gene expression by switching
NPR1's association with the WRKY transcription repressors to
TGA transcription activators. Sumoylation also triggers NPR1
degradation, rendering the immune induction transient. SUMO
modification of NPR1 is inhibited by phosphorylation at
Ser55/Ser59, which keeps NPR1 stable and quiescent. Thus,
posttranslational modifications enable dynamic but tight and
precise control of plant immune responses.},
Doi = {10.1016/j.chom.2015.07.005},
Key = {fds322291}
}
@article{fds228274,
Author = {Gu, Y and Dong, X},
Title = {Stromules: Signal Conduits for Plant Immunity.},
Journal = {Developmental cell},
Volume = {34},
Number = {1},
Pages = {3-4},
Year = {2015},
Month = {July},
ISSN = {1534-5807},
url = {http://dx.doi.org/10.1016/j.devcel.2015.06.018},
Abstract = {The chloroplast is a primary site for the production of
immune signals in plants. In this issue of Developmental
Cell, Caplan et al. (2015) report that chloroplasts send out
stromules as signal conduits for transmission of these
immune signals to the nucleus during effector-triggered
immunity.},
Doi = {10.1016/j.devcel.2015.06.018},
Key = {fds228274}
}
@article{fds228275,
Author = {Zheng, X-Y and Zhou, M and Yoo, H and Pruneda-Paz, JL and Spivey, NW and Kay, SA and Dong, X},
Title = {Spatial and temporal regulation of biosynthesis of the plant
immune signal salicylic acid.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {112},
Number = {30},
Pages = {9166-9173},
Year = {2015},
Month = {July},
ISSN = {0027-8424},
url = {http://dx.doi.org/10.1073/pnas.1511182112},
Abstract = {The plant hormone salicylic acid (SA) is essential for local
defense and systemic acquired resistance (SAR). When plants,
such as Arabidopsis, are challenged by different pathogens,
an increase in SA biosynthesis generally occurs through
transcriptional induction of the key synthetic enzyme
isochorismate synthase 1 (ICS1). However, the regulatory
mechanism for this induction is poorly understood. Using a
yeast one-hybrid screen, we identified two transcription
factors (TFs), NTM1-like 9 (NTL9) and CCA1 hiking expedition
(CHE), as activators of ICS1 during specific immune
responses. NTL9 is essential for inducing ICS1 and two other
SA synthesis-related genes, phytoalexin-deficient 4 (PAD4)
and enhanced disease susceptibility 1 (EDS1), in guard cells
that form stomata. Stomata can quickly close upon challenge
to block pathogen entry. This stomatal immunity requires
ICS1 and the SA signaling pathway. In the ntl9 mutant, this
response is defective and can be rescued by exogenous
application of SA, indicating that NTL9-mediated SA
synthesis is essential for stomatal immunity. CHE, the
second identified TF, is a central circadian clock
oscillator and is required not only for the daily
oscillation in SA levels but also for the pathogen-induced
SA synthesis in systemic tissues during SAR. CHE may also
regulate ICS1 through the known transcription activators
calmodulin binding protein 60g (CBP60g) and systemic
acquired resistance deficient 1 (SARD1) because induction of
these TF genes is compromised in the che-2 mutant. Our study
shows that SA biosynthesis is regulated by multiple TFs in a
spatial and temporal manner and therefore fills a gap in the
signal transduction pathway between pathogen recognition and
SA production.},
Doi = {10.1073/pnas.1511182112},
Key = {fds228275}
}
@article{fds228277,
Author = {Zhou, M and Wang, W and Karapetyan, S and Mwimba, M and Marques, J and Buchler, NE and Dong, X},
Title = {Redox rhythm reinforces the circadian clock to gate immune
response},
Journal = {Nature},
Volume = {advance online publication},
Number = {7561},
Pages = {472-476},
Publisher = {Nature Publishing Group, a division of Macmillan Publishers
Limited. All Rights Reserved.},
Year = {2015},
Month = {June},
ISSN = {0028-0836},
url = {http://hdl.handle.net/10161/10230 Duke open
access},
Abstract = {Recent studies have shown that in addition to the
transcriptional circadian clock, many organisms, including
Arabidopsis, have a circadian redox rhythm driven by the
organism's metabolic activities. It has been hypothesized
that the redox rhythm is linked to the circadian clock, but
the mechanism and the biological significance of this link
have only begun to be investigated. Here we report that the
master immune regulator NPR1 (non-expressor of
pathogenesis-related gene 1) of Arabidopsis is a sensor of
the plant's redox state and regulates transcription of core
circadian clock genes even in the absence of pathogen
challenge. Surprisingly, acute perturbation in the redox
status triggered by the immune signal salicylic acid does
not compromise the circadian clock but rather leads to its
reinforcement. Mathematical modelling and subsequent
experiments show that NPR1 reinforces the circadian clock
without changing the period by regulating both the morning
and the evening clock genes. This balanced network
architecture helps plants gate their immune responses
towards the morning and minimize costs on growth at night.
Our study demonstrates how a sensitive redox rhythm
interacts with a robust circadian clock to ensure proper
responsiveness to environmental stimuli without compromising
fitness of the organism.},
Doi = {10.1038/nature14449},
Key = {fds228277}
}
@article{fds228276,
Author = {Yang, L and Li, B and Zheng, X-Y and Li, J and Yang, M and Dong, X and He, G and An, C and Deng, XW},
Title = {Salicylic acid biosynthesis is enhanced and contributes to
increased biotrophic pathogen resistance in Arabidopsis
hybrids.},
Journal = {Nature communications},
Volume = {6},
Pages = {7309},
Year = {2015},
Month = {June},
url = {http://hdl.handle.net/10161/10360 Duke open
access},
Abstract = {Heterosis, the phenotypic superiority of a hybrid over its
parents, has been demonstrated for many traits in
Arabidopsis thaliana, but its effect on defence remains
largely unexplored. Here, we show that hybrids between some
A. thaliana accessions show increased resistance to the
biotrophic bacterial pathogen Pseudomonas syringae pv.
tomato (Pst) DC3000. Comparisons of transcriptomes between
these hybrids and their parents after inoculation reveal
that several key salicylic acid (SA) biosynthesis genes are
significantly upregulated in hybrids. Moreover, SA levels
are higher in hybrids than in either parent. Increased
resistance to Pst DC3000 is significantly compromised in
hybrids of pad4 mutants in which the SA biosynthesis pathway
is blocked. Finally, increased histone H3 acetylation of key
SA biosynthesis genes correlates with their upregulation in
infected hybrids. Our data demonstrate that enhanced
activation of SA biosynthesis in A. thaliana hybrids may
contribute to their increased resistance to a biotrophic
bacterial pathogen.},
Doi = {10.1038/ncomms8309},
Key = {fds228276}
}
@article{fds228280,
Author = {Mammarella, ND and Cheng, Z and Fu, ZQ and Daudi, A and Bolwell, GP and Dong, X and Ausubel, FM},
Title = {Apoplastic peroxidases are required for salicylic
acid-mediated defense against Pseudomonas
syringae.},
Journal = {Phytochemistry},
Volume = {112},
Pages = {110-121},
Year = {2015},
Month = {April},
ISSN = {0031-9422},
url = {http://dx.doi.org/10.1016/j.phytochem.2014.07.010},
Abstract = {Reactive oxygen species (ROS) generated by NADPH oxidases or
apoplastic peroxidases play an important role in the plant
defense response. Diminished expression of at least two
Arabidopsis thaliana peroxidase encoding genes, PRX33
(At3g49110) and PRX34 (At3g49120), as a consequence of
anti-sense expression of a heterologous French bean
peroxidase gene (asFBP1.1), were previously shown to result
in reduced levels of ROS following pathogen attack, enhanced
susceptibility to a variety of bacterial and fungal
pathogens, and reduced levels of callose production and
defense-related gene expression in response to the microbe
associated molecular pattern (MAMP) molecules flg22 and
elf26. These data demonstrated that the peroxidase-dependent
oxidative burst plays an important role in the elicitation
of pattern-triggered immunity (PTI). Further work reported
in this paper, however, shows that asFBP1.1 antisense plants
are not impaired in all PTI-associated responses. For
example, some but not all flg22-elicited genes are induced
to lower levels by flg22 in asFPB1.1, and callose deposition
in asFPB1.1 is similar to wild-type following infiltration
with a Pseudomonas syringae hrcC mutant or with non-host P.
syringae pathovars. Moreover, asFPB1.1 plants did not
exhibit any apparent defect in their ability to mount a
hypersensitive response (HR). On the other hand, salicylic
acid (SA)-mediated activation of PR1 was dramatically
impaired in asFPB1.1 plants. In addition, P.
syringae-elicited expression of many genes known to be
SA-dependent was significantly reduced in asFBP1.1 plants.
Consistent with this latter result, in asFBP1.1 plants the
key regulator of SA-mediated responses, NPR1, showed both
dramatically decreased total protein abundance and a failure
to monomerize, which is required for its translocation into
the nucleus.},
Doi = {10.1016/j.phytochem.2014.07.010},
Key = {fds228280}
}
@article{fds228278,
Author = {Wang, S and Gu, Y and Zebell, SG and Anderson, LK and Wang, W and Mohan, R and Dong, X},
Title = {A noncanonical role for the CKI-RB-E2F cell-cycle signaling
pathway in plant effector-triggered immunity.},
Journal = {Cell host & microbe},
Volume = {16},
Number = {6},
Pages = {787-794},
Year = {2014},
Month = {December},
ISSN = {1931-3128},
url = {http://dx.doi.org/10.1016/j.chom.2014.10.005},
Abstract = {Effector-triggered immunity (ETI), the major host defense
mechanism in plants, is often associated with programmed
cell death (PCD). Plants lack close homologs of caspases,
the key mediators of PCD in animals. So although the NB-LRR
receptors involved in ETI are well studied, how they
activate PCD and confer disease resistance remains elusive.
We show that the Arabidopsis nuclear envelope protein, CPR5,
negatively regulates ETI and the associated PCD through a
physical interaction with cyclin-dependent kinase inhibitors
(CKIs). Upon ETI induction, CKIs are released from CPR5 to
cause overactivation of another core cell-cycle regulator,
E2F. In cki and e2f mutants, ETI responses induced by both
TIR-NB-LRR and CC-NB-LRR classes of immune receptors are
compromised. We further show that E2F is deregulated during
ETI, probably through CKI-mediated hyperphosphorylation of
retinoblastoma-related 1 (RBR1). This study demonstrates
that canonical cell-cycle regulators also play important
noncanonical roles in plant immunity.},
Doi = {10.1016/j.chom.2014.10.005},
Key = {fds228278}
}
@article{fds228281,
Author = {Yan, S and Dong, X},
Title = {Perception of the plant immune signal salicylic
acid.},
Journal = {Current opinion in plant biology},
Volume = {20},
Pages = {64-68},
Year = {2014},
Month = {August},
ISSN = {1369-5266},
url = {http://dx.doi.org/10.1016/j.pbi.2014.04.006},
Abstract = {Salicylic acid (SA) plays a central role in plant innate
immunity. The diverse functions of this simple phenolic
compound suggest that plants may have multiple SA receptors.
Several SA-binding proteins have been identified using
biochemical approaches. However, genetic evidence supporting
that they are the bona fide SA receptors has not been
forthcoming. Mutant screens revealed that NPR1 is a master
regulator of SA-mediated responses. Although NPR1 cannot
bind SA in a conventional ligand-binding assay, its homologs
NPR3 and NPR4 bind SA and function as SA receptors. During
pathogen challenge, the SA gradient generated at the
infection site is sensed by NPR3 and NPR4, which serve as
the adaptors for the Cullin 3-based E3 ubiquitin ligase to
regulate NPR1 degradation. Consequently, NPR1 is degraded at
the infection site to remove its inhibition on
effector-triggered cell death and defense, whereas NPR1
accumulates in neighboring cells to promote cell survival
and SA-mediated resistance.},
Doi = {10.1016/j.pbi.2014.04.006},
Key = {fds228281}
}
@article{fds228279,
Author = {Fonseca, JP and Dong, X},
Title = {Functional characterization of a Nudix hydrolase AtNUDX8
upon pathogen attack indicates a positive role in plant
immune responses.},
Journal = {PloS one},
Volume = {9},
Number = {12},
Pages = {e114119},
Year = {2014},
Month = {January},
url = {http://dx.doi.org/10.1371/journal.pone.0114119},
Abstract = {Nudix hydrolases comprise a large gene family of twenty nine
members in Arabidopsis, each containing a conserved motif
capable of hydrolyzing specific substrates like ADP-glucose
and NADH. Until now only two members of this family, AtNUDX6
and AtNUDX7, have been shown to be involved in plant
immunity. RPP4 is a resistance gene from a multigene family
that confers resistance to downy mildew. A time course
expression profiling after Hyaloperonospora arabidopsidis
inoculation in both wild-type (WT) and the rpp4 mutant was
carried out to identify differentially expressed genes in
RPP4-mediated resistance. AtNUDX8 was one of several
differentially expressed, downregulated genes identified. A
T-DNA knockout mutant (KO-nudx8) was obtained from a Salk
T-DNA insertion collection, which exhibited abolished
AtNUDX8 expression. The KO-nudx8 mutant was infected
separately from the oomycete pathogen Hpa and the bacterial
pathogen Pseudomonas syringae pv. maculicola ES4326. The
mutant displayed a significantly enhanced disease
susceptibility to both pathogens when compared with the WT
control. We observed a small, stunted phenotype for KO-nudx8
mutant plants when grown over a 12/12 hour photoperiod but
not over a 16/8 hour photoperiod. AtNUDX8 expression peaked
at 8 hours after the lights were turned on and this
expression was significantly repressed four-fold by
salicylic acid (SA). The expression of three
pathogen-responsive thioredoxins (TRX-h2, TRX-h3 and TRX-h5)
were downregulated at specific time points in the KO-nudx8
mutant when compared with the WT. Furthermore, KO-nudx8
plants like the npr1 mutant, displayed SA hypersensitivity.
Expression of a key SA biosynthetic gene ICS1 was repressed
at specific time points in the KO-nudx8 mutant suggesting
that AtNUDX8 is involved in SA signaling in plants.
Similarly, NPR1 and PR1 transcript levels were also
downregulated at specific time points in the KO-nudx8
mutant. This study shows that AtNUDX8 is involved in plant
immunity as a positive regulator of defense in
Arabidopsis.},
Doi = {10.1371/journal.pone.0114119},
Key = {fds228279}
}
@article{fds228283,
Author = {Yan, S and Wang, W and Marqués, J and Mohan, R and Saleh, A and Durrant,
WE and Song, J and Dong, X},
Title = {Salicylic acid activates DNA damage responses to potentiate
plant immunity.},
Journal = {Molecular cell},
Volume = {52},
Number = {4},
Pages = {602-610},
Year = {2013},
Month = {November},
ISSN = {1097-2765},
url = {http://dx.doi.org/10.1016/j.molcel.2013.09.019},
Abstract = {DNA damage is normally detrimental to living organisms. Here
we show that it can also serve as a signal to promote immune
responses in plants. We found that the plant immune hormone
salicylic acid (SA) can trigger DNA damage in the absence of
a genotoxic agent. The DNA damage sensor proteins RAD17 and
ATR are required for effective immune responses. These
sensor proteins are negatively regulated by a key immune
regulator, SNI1 (suppressor of npr1-1, inducible 1), which
we found is a subunit of the structural maintenance of
chromosome (SMC) 5/6 complex required for controlling DNA
damage. Elevated DNA damage caused by the sni1 mutation or
treatment with a DNA-damaging agent markedly enhances
SA-mediated defense gene expression. Our study suggests that
activation of DNA damage responses is an intrinsic component
of the plant immune responses.},
Language = {eng},
Doi = {10.1016/j.molcel.2013.09.019},
Key = {fds228283}
}
@article{fds228284,
Author = {Chen, X and Barnaby, JY and Sreedharan, A and Huang, X and Orbović, V and Grosser, JW and Wang, N and Dong, X and Song, WY},
Title = {Over-expression of the citrus gene CtNH1 confers resistance
to bacterial canker disease},
Journal = {Physiological and Molecular Plant Pathology},
Volume = {84},
Number = {1},
Pages = {115-122},
Publisher = {Elsevier BV},
Year = {2013},
Month = {October},
ISSN = {0885-5765},
url = {http://www.sciencedirect.com/science/article/pii/S0885576513000477},
Abstract = {Citrus canker is a devastating disease, caused by
Xanthomonas axonopodis pv. citri (Xac). It is well
established that the NPR1 gene plays a pivotal role in
systemic acquired resistance (SAR) in Arabidopsis. In this
study, we report the isolation and characterization of an
NPR1 homolog from citrus, namely Citrus NPR1 homolog 1
(CtNH1). Sequence alignment and phylogenetic analysis
indicate that CtNH1 is closely-related to the Arabidopsis
NPR1 gene and its orthologs from rice, grapevine, and cacao.
When over-expressed in citrus, CtNH1 confers resistance to
Xac and leads to constitutive expression of the
pathogenesis-related (PR) gene chitinase 1 (Chi1),
suggesting that CtNH1 is orthologous to NPR1. ©
2013.},
Doi = {10.1016/j.pmpp.2013.07.002},
Key = {fds228284}
}
@article{fds228285,
Author = {Fu, ZQ and Dong, X},
Title = {Systemic acquired resistance: turning local infection into
global defense.},
Journal = {Annual review of plant biology},
Volume = {64},
Pages = {839-863},
Year = {2013},
Month = {January},
url = {http://www.ncbi.nlm.nih.gov/pubmed/23373699},
Abstract = {Systemic acquired resistance (SAR) is an induced immune
mechanism in plants. Unlike vertebrate adaptive immunity,
SAR is broad spectrum, with no specificity to the initial
infection. An avirulent pathogen causing local programmed
cell death can induce SAR through generation of mobile
signals, accumulation of the defense hormone salicylic acid,
and secretion of the antimicrobial PR (pathogenesis-related)
proteins. Consequently, the rest of the plant is protected
from secondary infection for a period of weeks to months.
SAR can even be passed on to progeny through epigenetic
regulation. The Arabidopsis NPR1 (nonexpresser of PR genes
1) protein is a master regulator of SAR. Recent study has
shown that salicylic acid directly binds to the NPR1 adaptor
proteins NPR3 and NPR4, regulates their interactions with
NPR1, and controls NPR1 protein stability. However, how NPR1
interacts with TGA transcription factors to activate defense
gene expression is still not well understood. In addition,
redox regulators, the mediator complex, WRKY transcription
factors, endoplasmic reticulum-resident proteins, and DNA
repair proteins play critical roles in SAR.},
Doi = {10.1146/annurev-arplant-042811-105606},
Key = {fds228285}
}
@article{fds228300,
Author = {Zheng, X-Y and Spivey, NW and Zeng, W and Liu, P-P and Fu, ZQ and Klessig,
DF and He, SY and Dong, X},
Title = {Coronatine promotes Pseudomonas syringae virulence in plants
by activating a signaling cascade that inhibits salicylic
acid accumulation.},
Journal = {Cell host & microbe},
Volume = {11},
Number = {6},
Pages = {587-596},
Year = {2012},
Month = {June},
ISSN = {1934-6069},
url = {http://www.ncbi.nlm.nih.gov/pubmed/22704619},
Keywords = {Amino Acids • Arabidopsis • Indenes • Plant
Diseases • Plant Proteins • Pseudomonas syringae
• Salicylic Acid • Signal Transduction* •
Transcriptional Activation • Virulence • Virulence
Factors • metabolism • metabolism* •
microbiology • microbiology* • pathogenicity*
• toxicity*},
Abstract = {Phytopathogens can manipulate plant hormone signaling to
access nutrients and counteract defense responses.
Pseudomonas syringae produces coronatine, a toxin that
mimics the plant hormone jasmonic acid isoleucine and
promotes opening of stomata for bacterial entry, bacterial
growth in the apoplast, systemic susceptibility, and disease
symptoms. We examined the mechanisms underlying
coronatine-mediated virulence and show that coronatine
activates three homologous NAC transcription factor (TF)
genes, ANAC019, ANAC055, and ANAC072, through direct
activity of the TF, MYC2. Genetic characterization of NAC TF
mutants demonstrates that these TFs mediate
coronatine-induced stomatal reopening and bacterial
propagation in both local and systemic tissues by inhibiting
the accumulation of the key plant immune signal salicylic
acid (SA). These NAC TFs exert this inhibitory effect by
repressing ICS1 and activating BSMT1, genes involved in SA
biosynthesis and metabolism, respectively. Thus, a signaling
cascade by which coronatine confers its multiple virulence
activities has been elucidated.},
Language = {eng},
Doi = {10.1016/j.chom.2012.04.014},
Key = {fds228300}
}
@article{fds228299,
Author = {Fu, ZQ and Yan, S and Saleh, A and Wang, W and Ruble, J and Oka, N and Mohan,
R and Spoel, SH and Tada, Y and Zheng, N and Dong, X},
Title = {NPR3 and NPR4 are receptors for the immune signal salicylic
acid in plants.},
Journal = {Nature},
Volume = {486},
Number = {7402},
Pages = {228-232},
Year = {2012},
Month = {May},
ISSN = {1476-4687},
url = {http://www.ncbi.nlm.nih.gov/pubmed/22699612},
Keywords = {Arabidopsis • Arabidopsis Proteins • Mutation
• Protein Binding • Salicylic Acid • Signal
Transduction* • Two-Hybrid System Techniques •
Ubiquitin-Protein Ligases • genetics • genetics*
• immunology • metabolism •
metabolism*},
Abstract = {Salicylic acid (SA) is a plant immune signal produced after
pathogen challenge to induce systemic acquired resistance.
It is the only major plant hormone for which the receptor
has not been firmly identified. Systemic acquired resistance
in Arabidopsis requires the transcription cofactor
nonexpresser of PR genes 1 (NPR1), the degradation of which
acts as a molecular switch. Here we show that the NPR1
paralogues NPR3 and NPR4 are SA receptors that bind SA with
different affinities. NPR3 and NPR4 function as adaptors of
the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation
in an SA-regulated manner. Accordingly, the Arabidopsis
npr3 npr4 double mutant accumulates higher levels of NPR1,
and is insensitive to induction of systemic acquired
resistance. Moreover, this mutant is defective in pathogen
effector-triggered programmed cell death and immunity. Our
study reveals the mechanism of SA perception in determining
cell death and survival in response to pathogen
challenge.},
Language = {eng},
Doi = {10.1038/nature11162},
Key = {fds228299}
}
@article{fds228297,
Author = {Moreno, AA and Mukhtar, MS and Blanco, F and Boatwright, JL and Moreno,
I and Jordan, MR and Chen, Y and Brandizzi, F and Dong, X and Orellana, A and Pajerowska Mukhtar and KM},
Title = {IRE1/bZIP60-mediated unfolded protein response plays
distinct roles in plant immunity and abiotic stress
responses.},
Journal = {PloS one},
Volume = {7},
Number = {2},
Pages = {e31944},
Year = {2012},
Month = {February},
ISSN = {1932-6203},
url = {http://dx.doi.org/10.1371/journal.pone.0031944},
Keywords = {Arabidopsis • Arabidopsis Proteins • Basic-Leucine
Zipper Transcription Factors • Endoribonucleases •
Plant Immunity* • Protein Isoforms • Protein
Kinases • Transcription Factors • Transcriptional
Activation • Unfolded Protein Response* • genetics
• immunology • physiology*},
Abstract = {Endoplasmic reticulum (ER)-mediated protein secretion and
quality control have been shown to play an important role in
immune responses in both animals and plants. In mammals, the
ER membrane-located IRE1 kinase/endoribonuclease, a key
regulator of unfolded protein response (UPR), is required
for plasma cell development to accommodate massive secretion
of immunoglobulins. Plant cells can secrete the so-called
pathogenesis-related (PR) proteins with antimicrobial
activities upon pathogen challenge. However, whether IRE1
plays any role in plant immunity is not known. Arabidopsis
thaliana has two copies of IRE1, IRE1a and IRE1b. Here, we
show that both IRE1a and IRE1b are transcriptionally induced
during chemically-induced ER stress, bacterial pathogen
infection and treatment with the immune signal salicylic
acid (SA). However, we found that IRE1a plays a predominant
role in the secretion of PR proteins upon SA treatment.
Consequently, the ire1a mutant plants show enhanced
susceptibility to a bacterial pathogen and are deficient in
establishing systemic acquired resistance (SAR), whereas
ire1b is unaffected in these responses. We further
demonstrate that the immune deficiency in ire1a is due to a
defect in SA- and pathogen-triggered, IRE1-mediated
cytoplasmic splicing of the bZIP60 mRNA, which encodes a
transcription factor involved in the expression of
UPR-responsive genes. Consistently, IRE1a is preferentially
required for bZIP60 splicing upon pathogen infection, while
IRE1b plays a major role in bZIP60 processing upon
Tunicamycin (Tm)-induced stress. We also show that
SA-dependent induction of UPR-responsive genes is altered in
the bzip60 mutant resulting in a moderate susceptibility to
a bacterial pathogen. These results indicate that the
IRE1/bZIP60 branch of UPR is a part of the plant response to
pathogens for which the two Arabidopsis IRE1 isoforms play
only partially overlapping roles and that IRE1 has both
bZIP60-dependent and bZIP60-independent functions in plant
immunity.},
Language = {eng},
Doi = {10.1371/journal.pone.0031944},
Key = {fds228297}
}
@article{fds228296,
Author = {Spoel, SH and Dong, X},
Title = {How do plants achieve immunity? Defence without specialized
immune cells.},
Journal = {Nature reviews. Immunology},
Volume = {12},
Number = {2},
Pages = {89-100},
Year = {2012},
Month = {January},
ISSN = {1474-1733},
url = {http://dx.doi.org/10.1038/nri3141},
Abstract = {Vertebrates have evolved a sophisticated adaptive immune
system that relies on an almost infinite diversity of
antigen receptors that are clonally expressed by specialized
immune cells that roam the circulatory system. These immune
cells provide vertebrates with extraordinary
antigen-specific immune capacity and memory, while
minimizing self-reactivity. Plants, however, lack
specialized mobile immune cells. Instead, every plant cell
is thought to be capable of launching an effective immune
response. So how do plants achieve specific, self-tolerant
immunity and establish immune memory? Recent developments
point towards a multilayered plant innate immune system
comprised of self-surveillance, systemic signalling and
chromosomal changes that together establish effective
immunity.},
Doi = {10.1038/nri3141},
Key = {fds228296}
}
@article{fds228298,
Author = {Pajerowska-Mukhtar, KM and Wang, W and Tada, Y and Oka, N and Tucker,
CL and Fonseca, JP and Dong, X},
Title = {The HSF-like transcription factor TBF1 is a major molecular
switch for plant growth-to-defense transition.},
Journal = {Current biology : CB},
Volume = {22},
Number = {2},
Pages = {103-112},
Year = {2012},
Month = {January},
ISSN = {1879-0445},
url = {http://www.ncbi.nlm.nih.gov/pubmed/22244999},
Keywords = {Arabidopsis • Arabidopsis Proteins • DNA-Binding
Proteins • Gene Expression Regulation, Plant* •
Heat-Shock Proteins • Immunity, Innate* • Open
Reading Frames • Peptide Elongation Factor Tu •
Peptide Fragments • Plant Proteins • Promoter
Regions, Genetic • Salicylic Acid • Transcription
Factors • growth & development • immunology •
metabolism • metabolism*},
Abstract = {<h4>Background</h4>Induction of plant immune responses
involves significant transcription reprogramming that
prioritizes defense over growth-related cellular functions.
Despite intensive forward genetic screens and genome-wide
expression-profiling studies, a limited number of
transcription factors have been found that regulate this
transition.<h4>Results</h4>Using the endoplasmic-reticulum-resident
genes required for antimicrobial protein secretion as
markers, we identified a heat-shock factor-like
transcription factor that specifically binds to the TL1
(GAAGAAGAA) cis element required for the induction of these
genes. Surprisingly, plants lacking this TL1-binding factor,
TBF1, respond normally to heat stress but are compromised in
immune responses induced by salicylic acid and by
microbe-associated molecular pattern, elf18. Genome-wide
expression profiling indicates that TBF1 plays a key role in
the growth-to-defense transition. Moreover, the expression
of TBF1 itself is tightly regulated at both the
transcriptional and translational levels. Two upstream open
reading frames encoding multiple aromatic amino acids were
found 5' of the translation initiation codon of TBF1 and
shown to affect its translation.<h4>Conclusions</h4>Through
this unique regulatory mechanism, TBF1 can sense the
metabolic changes upon pathogen invasion and trigger the
specific transcriptional reprogramming through its target
genes expression.},
Language = {eng},
Doi = {10.1016/j.cub.2011.12.015},
Key = {fds228298}
}
@article{fds228301,
Author = {Cheng, YT and Li, Y and Huang, S and Huang, Y and Dong, X and Zhang, Y and Li,
X},
Title = {Stability of plant immune-receptor resistance proteins is
controlled by SKP1-CULLIN1-F-box (SCF)-mediated protein
degradation.},
Journal = {Proc Natl Acad Sci U S A},
Volume = {108},
Number = {35},
Pages = {14694-14699},
Year = {2011},
Month = {August},
ISSN = {0027-8424},
url = {http://dx.doi.org/10.1073/pnas.1105685108},
Keywords = {Arabidopsis Proteins • Autoimmunity • F-Box
Proteins • Immunity, Innate* • Mutation •
Phenotype • Plants • S-Phase Kinase-Associated
Proteins • immunology* • metabolism •
physiology • physiology*},
Abstract = {The nucleotide-binding domain and leucine-rich repeats
containing proteins (NLRs) serve as immune receptors in both
plants and animals. Overaccumulation of NLRs often leads to
autoimmune responses, suggesting that the levels of these
immune receptors must be tightly controlled. However, the
mechanism by which NLR protein levels are regulated is
unknown. Here we report that the F-box protein CPR1 controls
the stability of plant NLR resistance proteins.
Loss-of-function mutations in CPR1 lead to higher
accumulation of the NLR proteins SNC1 and RPS2, as well as
autoactivation of immune responses. The autoimmune responses
in cpr1 mutant plants can be largely suppressed by knocking
out SNC1. Furthermore, CPR1 interacts with SNC1 and RPS2 in
vivo, and overexpressing CPR1 results in reduced
accumulation of SNC1 and RPS2, as well as suppression of
immunity mediated by these two NLR proteins. Our data
suggest that SKP1-CULLIN1-F-box (SCF) complex-mediated
stability control of plant NLR proteins plays an important
role in regulating their protein levels and preventing
autoimmunity.},
Language = {eng},
Doi = {10.1073/pnas.1105685108},
Key = {fds228301}
}
@article{fds228302,
Author = {Wang, D and Dong, X},
Title = {A highway for war and peace: the secretory pathway in
plant-microbe interactions.},
Journal = {Molecular plant},
Volume = {4},
Number = {4},
Pages = {581-587},
Year = {2011},
Month = {July},
ISSN = {1674-2052},
url = {http://dx.doi.org/10.1093/mp/ssr053},
Abstract = {Secretion of proteins and other molecules is the primary
means by which a cell interacts with its surroundings. The
overall organization of the secretory system is remarkably
conserved among eukaryotes, and many of the components have
been investigated in detail in animal models. Plant cells,
because of their sessile lifestyle, are uniquely reliant on
the secretory pathway to respond to changes in their
environments, either abiotic, such as the absence of
nutrients, or biotic, such as the presence of predators or
pathogens. In particular, most plant pathogens are
extracellular, which demands a robust and efficient host
secretory system directed at the site of attack. Here, we
present a summary of recent advances in our understanding of
the molecular details of the secretory pathway during
plant-microbe interactions. Secretion is required not only
for the delivery of antimicrobial molecules, but also for
the biogenesis of cell surface sensors to detect microbes.
The deposition of extracellular material is important in the
defense against classical bacterial pathogens as well as in
the so-called 'non-host' resistance. Finally, boosting the
protein secretion capacity is vital for avoiding infection
as well as for achieving symbiosis, even though in the
latter case, the microbes are engulfed in intracellular
compartments. The emerging evidence indicates that secretion
provides an essential interface between plant hosts and
their associated microbial partners.},
Doi = {10.1093/mp/ssr053},
Key = {fds228302}
}
@article{fds228303,
Author = {Song, J and Durrant, WE and Wang, S and Yan, S and Tan, EH and Dong,
X},
Title = {DNA repair proteins are directly involved in regulation of
gene expression during plant immune response.},
Journal = {Cell host & microbe},
Volume = {9},
Number = {2},
Pages = {115-124},
Year = {2011},
Month = {February},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21320694},
Abstract = {Systemic acquired resistance (SAR), an inducible
plant-defense response to local infection, requires the
signaling molecule salicylic acid (SA) and the
transcriptional coactivator NPR1, with concerted activation
of pathogenesis-related (PR) genes. Arabidopsis sni1 is an
npr1 suppressor and derepression of defense genes in sni1
causes reduced growth and fertility and increased homologous
recombination. Characterizing suppressors of sni1, we
identify the DNA damage repair proteins SSN2 and RAD51D as
genetic and physical interactors with SNI1. During plant
defense, SSN2 and possibly RAD51D replace the transcription
repressor SNI1 at pathogenesis-related gene promoters. In
the presence of SNI1, NPR1 is also required for SSN2
binding. Thus, coordinated action of SNI1, SSN2-RAD51D, and
NPR1 ensures the tight control of plant immune gene
expression. Given that the SSN2-RAD51D complex is conserved
in eukaryotes, their dual function in homologous
recombination and transcription regulation of plant-defense
genes suggests a general link between these two stress
responses.},
Doi = {10.1016/j.chom.2011.01.011},
Key = {fds228303}
}
@article{fds228305,
Author = {Wang, W and Barnaby, JY and Tada, Y and Li, H and Tör, M and Caldelari, D and Lee, D-U and Fu, X-D and Dong, X},
Title = {Timing of plant immune responses by a central circadian
regulator.},
Journal = {Nature},
Volume = {470},
Number = {7332},
Pages = {110-114},
Year = {2011},
Month = {February},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21293378},
Abstract = {The principal immune mechanism against biotrophic pathogens
in plants is the resistance (R)-gene-mediated defence. It
was proposed to share components with the broad-spectrum
basal defence machinery. However, the underlying molecular
mechanism is largely unknown. Here we report the
identification of novel genes involved in R-gene-mediated
resistance against downy mildew in Arabidopsis and their
regulatory control by the circadian regulator, CIRCADIAN
CLOCK-ASSOCIATED 1 (CCA1). Numerical clustering based on
phenotypes of these gene mutants revealed that programmed
cell death (PCD) is the major contributor to resistance.
Mutants compromised in the R-gene-mediated PCD were also
defective in basal resistance, establishing an
interconnection between these two distinct defence
mechanisms. Surprisingly, we found that these new defence
genes are under circadian control by CCA1, allowing plants
to 'anticipate' infection at dawn when the pathogen normally
disperses the spores and time immune responses according to
the perception of different pathogenic signals upon
infection. Temporal control of the defence genes by CCA1
differentiates their involvement in basal and
R-gene-mediated defence. Our study has revealed a key
functional link between the circadian clock and plant
immunity.},
Doi = {10.1038/nature09766},
Key = {fds228305}
}
@article{fds303155,
Author = {Caldelari, D and Wang, G and Farmer, EE and Dong,
X},
Title = {Arabidopsis lox3 lox4 double mutants are male sterile and
defective in global proliferative arrest.},
Journal = {Plant molecular biology},
Volume = {75},
Number = {1-2},
Pages = {25-33},
Year = {2011},
Month = {January},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21052784},
Abstract = {Fertility and flower development are both controlled in part
by jasmonates, fatty acid-derived mediators produced via the
activity of 13-lipoxygenases (13-LOXs). The Arabidopsis
thaliana Columbia-0 reference genome is predicted to encode
four of these enzymes and it is already known that one of
these, LOX2, is dispensable for fertility. In this study,
the roles of the other three 13-LOXs (LOX3, LOX4 and LOX6)
were investigated in single and double mutants. Four
independent lox3 lox4 double mutants assembled with
different mutated lox3 and lox4 alleles had fully penetrant
floral phenotypes, displaying abnormal anther maturation and
defective dehiscence. The plants were no longer self-fertile
and pollen was not viable. Fertility in the double mutant
was restored genetically by complementation with either the
LOX3 or the LOX4 cDNAs and biochemically with exogenous
jasmonic acid. Furthermore, deficiency in LOX3 and LOX4
causes developmental dysfunctions, compared to wild type;
lox3 lox4 double mutants are taller and develop more
inflorescence shoots and flowers. Further analysis revealed
that developmental arrest in the lox3 lox4 inflorescence
occurs with the production of an abnormal carpelloid flower.
This distinguishes lox3 lox4 mutants from the wild type
where developmentally typical flower buds are the terminal
inflorescence structures observed in both the laboratory and
in nature. Our studies of lox3 lox4 as well as other
jasmonic acid biosynthesis and perception mutants show that
this plant hormone is not only required for male fertility
but also involved in global proliferative
arrest.},
Doi = {10.1007/s11103-010-9701-9},
Key = {fds303155}
}
@article{fds228304,
Author = {Caldelari, D and Wang, G and Farmer, EE and Dong,
X},
Title = {Inflorescence meristem arrest defects and male infertility
in Arabidopsis lox3 lox4 double mutants.},
Journal = {Plant Molecular Biology},
Volume = {75},
Number = {1-2},
Pages = {25-33},
Year = {2011},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21052784},
Abstract = {Fertility and flower development are both controlled in part
by jasmonates, fatty acid-derived mediators produced via the
activity of 13-lipoxygenases (13-LOXs). The Arabidopsis
thaliana Columbia-0 reference genome is predicted to encode
four of these enzymes and it is already known that one of
these, LOX2, is dispensable for fertility. In this study,
the roles of the other three 13-LOXs (LOX3, LOX4 and LOX6)
were investigated in single and double mutants. Four
independent lox3 lox4 double mutants assembled with
different mutated lox3 and lox4 alleles had fully penetrant
floral phenotypes, displaying abnormal anther maturation and
defective dehiscence. The plants were no longer self-fertile
and pollen was not viable. Fertility in the double mutant
was restored genetically by complementation with either the
LOX3 or the LOX4 cDNAs and biochemically with exogenous
jasmonic acid. Furthermore, deficiency in LOX3 and LOX4
causes developmental dysfunctions, compared to wild type;
lox3 lox4 double mutants are taller and develop more
inflorescence shoots and flowers. Further analysis revealed
that developmental arrest in the lox3 lox4 inflorescence
occurs with the production of an abnormal carpelloid flower.
This distinguishes lox3 lox4 mutants from the wild type
where developmentally typical flower buds are the terminal
inflorescence structures observed in both the laboratory and
in nature. Our studies of lox3 lox4 as well as other
jasmonic acid biosynthesis and perception mutants show that
this plant hormone is not only required for male fertility
but also involved in global proliferative
arrest.},
Doi = {10.1007/s11103-010-9701-9},
Key = {fds228304}
}
@article{fds228308,
Author = {Wang, S and Durrant, WE and Song, J and Spivey, NW and Dong,
X},
Title = {Arabidopsis BRCA2 and RAD51 proteins are specifically
involved in defense gene transcription during plant immune
responses.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {107},
Number = {52},
Pages = {22716-22721},
Year = {2010},
Month = {December},
url = {http://www.ncbi.nlm.nih.gov/pubmed/21149701},
Abstract = {Systemic acquired resistance (SAR) is a plant immune
response associated with both transcriptional reprogramming
and increased homologous DNA recombination (HR). SNI1 is a
negative regulator of SAR and HR, as indicated by the
increased basal expression of defense genes and HR in sni1.
We found that the sni1 phenotypes are rescued by mutations
in BREAST CANCER 2 (BRCA2). In humans, BRCA2 is a mediator
of RAD51 in pairing of homologous DNA. Mutations in BRCA2
cause predisposition to breast/ovarian cancers; however, the
role of the BRCA2-RAD51 complex in transcriptional
regulation remains unclear. In Arabidopsis, both brca2 and
rad51 were found to be hypersusceptible not only to
genotoxic substances, but also to pathogen infections. A
whole-genome microarray analysis showed that downstream of
NPR1, BRCA2A is a major regulator of defense-related gene
transcription. ChIP demonstrated that RAD51 is specifically
recruited to the promoters of defense genes during SAR. This
recruitment is dependent on the SAR signal salicylic acid
(SA) and on the function of BRCA2. This study provides the
molecular evidence showing that the BRCA2-RAD51 complex,
known for its function in HR, also plays a direct and
specific role in transcription regulation during plant
immune responses.},
Doi = {10.1073/pnas.1005978107},
Key = {fds228308}
}
@article{fds228309,
Author = {Pajerowska-Mukhtar, K and Dong, X},
Title = {A kiss of death--proteasome-mediated membrane fusion and
programmed cell death in plant defense against bacterial
infection.},
Journal = {Genes & development},
Volume = {23},
Number = {21},
Pages = {2449-2454},
Year = {2009},
Month = {November},
ISSN = {1549-5477},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19884251},
Abstract = {Eukaryotes have evolved various means for controlled and
organized cellular destruction, known as programmed cell
death (PCD). In plants, PCD is a crucial regulatory
mechanism in multiple physiological processes, including
terminal differentiation, senescence, and disease
resistance. In this issue of Genes & Development, Hatsugai
and colleagues (pp. 2496-2506) demonstrate a novel plant
defense strategy to trigger bacteria-induced PCD, involving
proteasome-dependent tonoplast and plasma membrane fusion
followed by discharge of vacuolar antimicrobial and
death-inducing contents into the apoplast.},
Doi = {10.1101/gad.1861609},
Key = {fds228309}
}
@article{fds228310,
Author = {Saijo, Y and Tintor, N and Lu, X and Rauf, P and Pajerowska-Mukhtar, K and Häweker, H and Dong, X and Robatzek, S and Schulze-Lefert,
P},
Title = {Receptor quality control in the endoplasmic reticulum for
plant innate immunity.},
Journal = {The EMBO journal},
Volume = {28},
Number = {21},
Pages = {3439-3449},
Year = {2009},
Month = {November},
ISSN = {0261-4189},
url = {http://dx.doi.org/10.1038/emboj.2009.263},
Abstract = {Pattern recognition receptors in eukaryotes initiate defence
responses on detection of microbe-associated molecular
patterns shared by many microbe species. The Leu-rich repeat
receptor-like kinases FLS2 and EFR recognize the bacterial
epitopes flg22 and elf18, derived from flagellin and
elongation factor-Tu, respectively. We describe Arabidopsis
'priority in sweet life' (psl) mutants that show
de-repressed anthocyanin accumulation in the presence of
elf18. EFR accumulation and signalling, but not of FLS2, are
impaired in psl1, psl2, and stt3a plants. PSL1 and PSL2,
respectively, encode calreticulin3 (CRT3) and
UDP-glucose:glycoprotein glycosyltransferase that act in
concert with STT3A-containing oligosaccharyltransferase
complex in an N-glycosylation pathway in the endoplasmic
reticulum. However, EFR-signalling function is impaired in
weak psl1 alleles despite its normal accumulation, thereby
uncoupling EFR abundance control from quality control.
Furthermore, salicylic acid-induced, but EFR-independent
defence is weakened in psl2 and stt3a plants, indicating the
existence of another client protein than EFR for this immune
response. Our findings suggest a critical and selective
function of N-glycosylation for different layers of plant
immunity, likely through quality control of
membrane-localized regulators.},
Doi = {10.1038/emboj.2009.263},
Key = {fds228310}
}
@article{fds228311,
Author = {Dong, X and Kahmann, R},
Title = {Battle for survival: plants and their allies and
enemies.},
Journal = {Current opinion in plant biology},
Volume = {12},
Number = {4},
Pages = {387-389},
Year = {2009},
Month = {August},
ISSN = {1369-5266},
url = {http://dx.doi.org/10.1016/j.pbi.2009.07.001},
Doi = {10.1016/j.pbi.2009.07.001},
Key = {fds228311}
}
@article{fds228312,
Author = {Spoel, SH and Mou, Z and Tada, Y and Spivey, NW and Genschik, P and Dong,
X},
Title = {Proteasome-mediated turnover of the transcription
coactivator NPR1 plays dual roles in regulating plant
immunity.},
Journal = {Cell},
Volume = {137},
Number = {5},
Pages = {860-872},
Year = {2009},
Month = {May},
ISSN = {1097-4172},
url = {http://www.ncbi.nlm.nih.gov/pubmed/19490895},
Abstract = {Systemic acquired resistance (SAR) is a broad-spectrum plant
immune response involving profound transcriptional changes
that are regulated by the coactivator NPR1. Nuclear
translocation of NPR1 is a critical regulatory step, but how
the protein is regulated in the nucleus is unknown. Here, we
show that turnover of nuclear NPR1 protein plays an
important role in modulating transcription of its target
genes. In the absence of pathogen challenge, NPR1 is
continuously cleared from the nucleus by the proteasome,
which restricts its coactivator activity to prevent untimely
activation of SAR. Surprisingly, inducers of SAR promote
NPR1 phosphorylation at residues Ser11/Ser15, and then
facilitate its recruitment to a Cullin3-based ubiquitin
ligase. Turnover of phosphorylated NPR1 is required for full
induction of target genes and establishment of SAR. These in
vivo data demonstrate dual roles for coactivator turnover in
both preventing and stimulating gene transcription to
regulate plant immunity.},
Doi = {10.1016/j.cell.2009.03.038},
Key = {fds228312}
}
@article{fds228294,
Author = {Spoel, SH and Dong, X},
Title = {Making sense of hormone crosstalk during
plant},
Journal = {Cell Host & Microbe},
Volume = {3},
Number = {6},
Pages = {348-351},
Year = {2008},
url = {http://dx.doi.org/10.1016/j.chom.2008.05.009},
Abstract = {In response to biotic stress, crosstalk between plant
hormonal signaling pathways prioritizes defense over other
cellular functions. Some plant pathogens take advantage of
this regulatory system by mimicking hormones that interfere
with host immune responses to promote virulence. Here we
discuss the various roles that crosstalk may play in
response to pathogens with different infection
strategies.},
Doi = {10.1016/j.chom.2008.05.009},
Key = {fds228294}
}
@article{fds228313,
Author = {Tada, Y and Spoel, SH and Pajerowska Mukhtar and K and Mou, Z and Song, J and Dong, X},
Title = {Plant Immunity Requires Conformational Changes of NPR1 via
S-Nitrosylation and Thioredoxins},
Journal = {Science},
Volume = {321},
Number = {5891},
Pages = {952-956},
Year = {2008},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18635760},
Abstract = {http://www.sciencemag.org/cgi/content/abstract/1156970?ijkey=/8he5p3s6CA6g&keytype=ref&siteid=sci},
Doi = {10.1126/science.1156970},
Key = {fds228313}
}
@article{fds228315,
Author = {Spoel, SH and Johnson, JS and Dong, X},
Title = {Regulation of tradeoffs between plant defenses against
pathogens with different lifestyles.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {104},
Number = {47},
Pages = {18842-18847},
Year = {2007},
Month = {November},
ISSN = {1091-6490},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17998535},
Abstract = {Plants activate distinct defense responses depending on the
lifestyle of the attacker encountered. In these responses,
salicylic acid (SA) and jasmonic acid (JA) play important
signaling roles. SA induces defense against biotrophic
pathogens that feed and reproduce on live host cells,
whereas JA activates defense against necrotrophic pathogens
that kill host cells for nutrition and reproduction.
Cross-talk between these defense signaling pathways has been
shown to optimize the response against a single attacker.
However, its role in defense against multiple pathogens with
distinct lifestyles is unknown. Here we show that infection
with biotrophic Pseudomonas syringae, which induces
SA-mediated defense, rendered plants more susceptible to the
necrotrophic pathogen Alternaria brassicicola by suppression
of the JA signaling pathway. This process was partly
dependent on the cross-talk modulator NPR1. Surprisingly,
this tradeoff was restricted to tissues adjacent to the site
of initial infection; A. brassicicola infection in systemic
tissue was not affected. Even more surprisingly, tradeoff
occurred only with the virulent Pseudomonas strain.
Avirulent strains that induced programmed cell death (PCD),
an effective plant-resistance mechanism against biotrophs,
did not cause suppression of JA-dependent defense. This
result might be advantageous to the plant by preventing
necrotrophic pathogen growth in tissues undergoing PCD. Our
findings show that plants tightly control cross-talk between
SA- and JA-dependent defenses in a previously unrecognized
spatial and pathogen type-specific fashion. This process
allows them to prevent unfavorable signal interactions and
maximize their ability to concomitantly fend off multiple
pathogens.},
Doi = {10.1073/pnas.0708139104},
Key = {fds228315}
}
@article{fds228316,
Author = {Wang, D and Pajerowska-Mukhtar, K and Culler, AH and Dong,
X},
Title = {Salicylic acid inhibits pathogen growth in plants through
repression of the auxin signaling pathway.},
Journal = {Current biology : CB},
Volume = {17},
Number = {20},
Pages = {1784-1790},
Year = {2007},
Month = {October},
ISSN = {0960-9822},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17919906},
Abstract = {The phytohormone auxin regulates almost every aspect of
plant development. At the molecular level, auxin induces
gene expression through direct physical interaction with the
TIR1-like F box proteins, which in turn remove the Aux/IAA
family of transcriptional repressors [1-4]. A growing body
of evidence indicates that many plant pathogens can either
produce auxin themselves or manipulate host auxin
biosynthesis to interfere with the host's normal
developmental processes [5-11]. In response, plants probably
evolved mechanisms to repress auxin signaling during
infection as a defense strategy. Plants overaccumulating the
defense signal molecule salicylic acid (SA) frequently
display morphological phenotypes that are reminiscent of
auxin-deficient or auxin-insensitive mutants, indicating
that SA might interfere with auxin responses. By using the
Affymetrix ATH1 GeneChip for Arabidopsis thaliana, we
performed a comprehensive study of the effects of SA on
auxin signaling [12]. We found that SA causes global
repression of auxin-related genes, including the TIR1
receptor gene, resulting in stabilization of the Aux/IAA
repressor proteins and inhibition of auxin responses. We
demonstrate that this inhibitory effect on auxin signaling
is a part of the SA-mediated disease-resistance
mechanism.},
Doi = {10.1016/j.cub.2007.09.025},
Key = {fds228316}
}
@article{fds228317,
Author = {Zhang, X and Dai, Y and Xiong, Y and Defraia, C and Li, J and Dong, X and Mou,
Z},
Title = {Overexpression of Arabidopsis MAP kinase kinase 7 leads to
activation of plant basal and systemic acquired
resistance.},
Journal = {Plant J},
Volume = {52},
Number = {6},
Pages = {1066-1079},
Year = {2007},
Month = {October},
ISSN = {0960-7412},
url = {http://dx.doi.org/10.1111/j.1365-313x.2007.03294.x},
Abstract = {There is a growing body of evidence indicating that
mitogen-activated protein kinase (MAPK) cascades are
involved in plant defense responses. Analysis of the
completed Arabidopsis thaliana genome sequence has revealed
the existence of 20 MAPKs, 10 MAPKKs and 60 MAPKKKs,
implying a high level of complexity in MAPK signaling
pathways, and making the assignment of gene functions
difficult. The MAP kinase kinase 7 (MKK7) gene of
Arabidopsis has previously been shown to negatively regulate
polar auxin transport. Here we provide evidence that MKK7
positively regulates plant basal and systemic acquired
resistance (SAR). The activation-tagged bud1 mutant, in
which the expression of MKK7 is increased, accumulates
elevated levels of salicylic acid (SA), exhibits
constitutive pathogenesis-related (PR) gene expression, and
displays enhanced resistance to both Pseudomonas syringae
pv. maculicola (Psm) ES4326 and Hyaloperonospora parasitica
Noco2. Both PR gene expression and disease resistance of the
bud1 plants depend on SA, and partially depend on NPR1. We
demonstrate that the constitutive defense response in bud1
plants is a result of the increased expression of MKK7, and
requires the kinase activity of the MKK7 protein. We found
that expression of the MKK7 gene in wild-type plants is
induced by pathogen infection. Reducing mRNA levels of MKK7
by antisense RNA expression not only compromises basal
resistance, but also blocks the induction of SAR.
Intriguingly, ectopic expression of MKK7 in local tissues
induces PR gene expression and resistance to Psm ES4326 in
systemic tissues, indicating that activation of MKK7 is
sufficient for generating the mobile signal of
SAR.},
Doi = {10.1111/j.1365-313x.2007.03294.x},
Key = {fds228317}
}
@article{fds228314,
Author = {Xue, C and Tada, Y and Dong, X and Heitman, J},
Title = {The human fungal pathogen Cryptococcus can complete its
sexual cycle during a pathogenic association with
plants.},
Journal = {Cell Host Microbe},
Volume = {1},
Number = {4},
Pages = {263-273},
Year = {2007},
Month = {June},
ISSN = {1934-6069},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18005707},
Abstract = {Cryptococcus is a globally distributed human fungal pathogen
that primarily afflicts immunocompromised individuals. How
and why this human fungal pathogen associates with plants
and how this environmental niche influences its life cycle
remains a mystery. We established Cryptococcus-Arabidopsis
and Cryptococcus-Eucalyptus systems and discovered that
Cryptococcus proliferates and mates on plant surfaces.
Mating efficiency of C. gattii was markedly enhanced on
plants and myo-inositol and indole acetic acid were specific
plant products that stimulated mating. On Arabidopsis,
dwarfing and chlorosis were observed following infection
with a fungal mixture of two opposite mating-type strains,
but not with either mating-type alone. This infection
process is countered by the plant jasmonate-mediated defense
mechanism. These findings reveal that Cryptococcus can
parasitically interact with plants to complete its sexual
cycle, which may impact an understanding of the origin and
evolution of both plant and animal fungal pathogens in
nature.},
Doi = {10.1016/j.chom.2007.05.005},
Key = {fds228314}
}
@article{fds228318,
Author = {Kesarwani, M and Yoo, J and Dong, X},
Title = {Genetic interactions of TGA transcription factors in the
regulation of pathogenesis-related genes and disease
resistance in Arabidopsis.},
Journal = {Plant physiology},
Volume = {144},
Number = {1},
Pages = {336-346},
Year = {2007},
Month = {May},
ISSN = {0032-0889},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17369431},
Keywords = {Arabidopsis • Arabidopsis Proteins • Gene
Expression Regulation, Plant • Immunity, Natural •
Models, Genetic • Mutagenesis, Insertional •
Mutation • Nuclear Proteins • Plant Diseases
• Plant Proteins • Transcription Factors •
genetics • genetics* • metabolism •
microbiology • physiology • physiology*},
Abstract = {TGA transcription factors are implicated as regulators of
pathogenesis-related (PR) genes because of their physical
interaction with the known positive regulator, nonexpresser
of PR gene1 (NPR1). A triple-knockout mutant tga2-1 tga5-1
tga6-1 was shown previously to be defective in the induction
of PR genes and systemic acquired resistance, confirming
their role in disease resistance. However, the contributions
of individual TGA factors have been difficult to discern
because of functional redundancy among these factors, as
well as possible dual functions for some single factors. In
this study, we characterized six TGA factors by reverse
genetics. We show that TGA3 is required for both basal and
2,6-dichloroisonicotinic acid-induced transcription of PR
genes. The tga3-1 mutants were found to be defective in
basal pathogen resistance, whereas induced resistance was
unaffected. TGA1 and TGA4 play partially redundant roles in
regulation of basal resistance, having only moderate effects
on PR gene expression. Additionally, an activation-tagged
mutant of TGA6 was able to increase basal as well as induced
expression of PR1, demonstrating a positive role for TGA6 on
PR gene expression. In contrast, TGA2 has repressor activity
on PR gene expression even though it can act as a positive
regulator in the tga5-1 tga6-1 null mutant background.
Finally, we examined the genetic interaction between tga2-2
and suppressor of npr1 inducible1 (sni1-1). TGA2's repressor
activity overlaps with SNI1 because the tga2-2 sni1-1 double
mutant shows a synergistic effect on PR gene
expression.},
Doi = {10.1104/pp.106.095299},
Key = {fds228318}
}
@article{fds228293,
Author = {Durrant, WE and Wang, S and Dong, X},
Title = {Erratum: Arabidopsis SNI1 and RAD51D regulate both gene
transcription and DNA recombination during the defense
response (Proceedings of the National Academy of Sciences of
the United States of America (2007) 104, 10, (4223-4227)
DOI: 10.1073/pnas.0609357104)},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {104},
Number = {17},
Pages = {7307},
Publisher = {Proceedings of the National Academy of Sciences},
Year = {2007},
Month = {April},
ISSN = {0027-8424},
url = {http://dx.doi.org/10.1073/pnas.0702347104},
Doi = {10.1073/pnas.0702347104},
Key = {fds228293}
}
@article{fds228306,
Author = {Durrant, WE and Wang, S and Dong, X},
Title = {Arabidopsis SNI1 and RAD51D regulate both gene transcription
and DNA recombination during the defense
response.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {104},
Number = {10},
Pages = {4223-4227},
Year = {2007},
Month = {March},
ISSN = {0027-8424},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17360504},
Keywords = {Amino Acid Sequence • Arabidopsis • Arabidopsis
Proteins • Chromosome Mapping • DNA Damage •
DNA* • DNA-Binding Proteins • Genetic
Predisposition to Disease • Models, Biological •
Molecular Sequence Data • Mutation* • Nuclear
Proteins • Phenotype • Plant Diseases •
Recombination, Genetic* • Transcription, Genetic*
• genetics* • physiology*},
Abstract = {The plant immune response known as systemic acquired
resistance (SAR) is a general defense mechanism that confers
long-lasting resistance against a broad spectrum of
pathogens. SAR triggers many molecular changes including
accumulation of antimicrobial pathogenesis-related (PR)
proteins. Transcription of PR genes in Arabidopsis is
regulated by the coactivator NPR1 and the repressor SNI1.
Pathogen infection also triggers an increase in somatic DNA
recombination, which results in transmission of changes to
the offspring of infected plants. However, it is not known
how the induction of homologous recombination during SAR is
controlled. Here, we show that SNI1 and RAD51D regulate both
gene expression and DNA recombination. In a genetic screen
for suppressors of sni1, we discovered that RAD51D is
required for NPR1-independent PR gene expression. As a
result, the rad51d mutant has enhanced disease
susceptibility. Besides altered PR gene expression, rad51d
plants are hypersensitive to DNA-damaging agents and are
impaired in homologous recombination. The dual role of
RAD51D and SNI1 in PR gene transcription and DNA
recombination suggests a mechanistic link between the
short-term defense response and a long-term survival
strategy.},
Doi = {10.1073/pnas.0609357104},
Key = {fds228306}
}
@article{fds228319,
Author = {Wang, D and Amornsiripanitch, N and Dong, X},
Title = {A genomic approach to identify regulatory nodes in the
transcriptional network of systemic acquired resistance in
plants.},
Journal = {PLoS pathogens},
Volume = {2},
Number = {11},
Pages = {e123},
Publisher = {Public Library of Science (PLoS)},
Year = {2006},
Month = {November},
ISSN = {1553-7374},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17096590},
Abstract = {Many biological processes are controlled by intricate
networks of transcriptional regulators. With the development
of microarray technology, transcriptional changes can be
examined at the whole-genome level. However, such analysis
often lacks information on the hierarchical relationship
between components of a given system. Systemic acquired
resistance (SAR) is an inducible plant defense response
involving a cascade of transcriptional events induced by
salicylic acid through the transcription cofactor NPR1. To
identify additional regulatory nodes in the SAR network, we
performed microarray analysis on Arabidopsis plants
expressing the NPR1-GR (glucocorticoid receptor) fusion
protein. Since nuclear translocation of NPR1-GR requires
dexamethasone, we were able to control NPR1-dependent
transcription and identify direct transcriptional targets of
NPR1. We show that NPR1 directly upregulates the expression
of eight WRKY transcription factor genes. This large family
of 74 transcription factors has been implicated in various
defense responses, but no specific WRKY factor has been
placed in the SAR network. Identification of NPR1-regulated
WRKY factors allowed us to perform in-depth genetic analysis
on a small number of WRKY factors and test well-defined
phenotypes of single and double mutants associated with
NPR1. Among these WRKY factors we found both positive and
negative regulators of SAR. This genomics-directed approach
unambiguously positioned five WRKY factors in the complex
transcriptional regulatory network of SAR. Our work not only
discovered new transcription regulatory components in the
signaling network of SAR but also demonstrated that
functional studies of large gene families have to take into
consideration sequence similarity as well as the expression
patterns of the candidates.},
Doi = {10.1371/journal.ppat.0020123},
Key = {fds228319}
}
@article{fds228320,
Author = {Heidel, AJ and Dong, X},
Title = {Fitness benefits of systemic acquired resistance during
Hyaloperonospora parasitica infection in Arabidopsis
thaliana.},
Journal = {Genetics},
Volume = {173},
Number = {3},
Pages = {1621-1628},
Year = {2006},
Month = {July},
ISSN = {0016-6731},
url = {http://www.ncbi.nlm.nih.gov/pubmed/16648642},
Abstract = {We investigated the fitness benefits of systemic acquired
resistance (SAR) in Arabidopsis thaliana using a mutational
and transformational genetic approach. Genetic lines were
designed to differ in the genes determining resistance
signaling in a common genetic background. Two mutant lines
(cpr1 and cpr5) constitutively activate SAR at different
points in SAR signaling, and one mutant line (npr1) has
impaired SAR. The transgenic line (NPR1-H) has enhanced
resistance when SAR is activated, but SAR is still inducible
similarly to wild type. The fitness benefits were also
investigated under two nutrient levels to test theories that
preventing pathogen damage and realized resistance benefits
may be affected by nutrient availability. Under low-nutrient
conditions and treatment with the pathogenic oomycete,
Hyaloperonospora parasitica, wild type had a higher fitness
than the mutant that could not activate SAR, demonstrating
that normal inducible SAR is beneficial in these conditions;
this result, however, was not found under high-nutrient
conditions. The mutants with constitutive SAR all failed to
show a fitness benefit in comparison to wild type under a H.
parasitica pathogen treatment, suggesting that SAR is
induced to prevent an excessive fitness cost.},
Doi = {10.1534/genetics.106.059022},
Key = {fds228320}
}
@article{fds228321,
Author = {Mosher, RA and Durrant, WE and Wang, D and Song, J and Dong,
X},
Title = {A comprehensive structure-function analysis of Arabidopsis
SNI1 defines essential regions and transcriptional repressor
activity.},
Journal = {The Plant cell},
Volume = {18},
Number = {7},
Pages = {1750-1765},
Year = {2006},
Month = {July},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/16766691},
Abstract = {The expression of systemic acquired resistance (SAR) in
plants involves the upregulation of many
Pathogenesis-Related (PR) genes, which work in concert to
confer resistance to a broad spectrum of pathogens. Because
SAR is a costly process, SAR-associated transcription must
be tightly regulated. Arabidopsis thaliana SNI1 (for
Suppressor of NPR1, Inducible) is a negative regulator of
SAR required to dampen the basal expression of PR genes.
Whole genome transcriptional profiling showed that in the
sni1 mutant, Nonexpresser of PR genes (NPR1)-dependent
benzothiadiazole S-methylester-responsive genes were
specifically derepressed. Interestingly, SNI1 also repressed
transcription when expressed in yeast, suggesting that it
functions as an active transcriptional repressor through a
highly conserved mechanism. Chromatin immunoprecipitation
indicated that histone modification may be involved in
SNI1-mediated repression. Sequence comparison with orthologs
in other plant species and a saturating NAAIRS-scanning
mutagenesis of SNI1 identified regions in SNI1 that are
required for its activity. The structural similarity of SNI1
to Armadillo repeat proteins implies that SNI1 may form a
scaffold for interaction with proteins that modulate
transcription.},
Doi = {10.1105/tpc.105.039677},
Key = {fds228321}
}
@article{fds228322,
Author = {Wang, D and Weaver, ND and Kesarwani, M and Dong,
X},
Title = {Induction of protein secretory pathway is required for
systemic acquired resistance.},
Journal = {Science (New York, N.Y.)},
Volume = {308},
Number = {5724},
Pages = {1036-1040},
Year = {2005},
Month = {May},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15890886},
Abstract = {In plants, systemic acquired resistance (SAR) is established
as a result of NPR1-regulated expression of
pathogenesis-related (PR) genes. Using gene expression
profiling in Arabidopsis, we found that in addition to
controlling the expression of PR genes, NPR1 also directly
controls the expression of the protein secretory pathway
genes. Up-regulation of these genes is essential for SAR,
because mutations in some of them diminished the secretion
of PR proteins (for example, PR1), resulting in reduced
resistance. We provide evidence that NPR1 coordinately
regulates these secretion-related genes through a previously
undescribed cis-element. Activation of this cis-element is
controlled by a transcription factor that is translocated
into the nucleus upon SAR induction.},
Doi = {10.1126/science.1108791},
Key = {fds228322}
}
@article{fds228323,
Author = {Heidel, AJ and Clarke, JD and Antonovics, J and Dong,
X},
Title = {Fitness costs of mutations affecting the systemic acquired
resistance pathway in Arabidopsis thaliana.},
Journal = {Genetics},
Volume = {168},
Number = {4},
Pages = {2197-2206},
Year = {2004},
Month = {December},
ISSN = {0016-6731},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15611186},
Abstract = {This study investigated the fitness effects of four
mutations (npr1, cpr1, cpr5, and cpr6) and two transgenic
genotypes (NPR1-L and NPR1-H) affecting different points of
the systemic acquired resistance (SAR) signaling pathway
associated with pathogen defense in Arabidopsis thaliana.
The npr1 mutation, which resulted in a failure to express
SAR, had no effect on fitness under growth chamber
conditions, but decreased fitness in the field. The
expression of NPR1 positively correlated with the fitness in
the field. Constitutive activation of SAR by cpr1, cpr5, and
cpr6 generally decreased fitness in the field and under two
nutrient levels in two growth chamber conditions. At
low-nutrient levels, fitness differences between wild type
and the constitutive mutants were unchanged or reduced
(especially in cpr5). The reduced fitness of the
constitutive mutants suggests that this pathway is costly,
with the precise fitness consequences highly dependent on
the environmental context.},
Doi = {10.1534/genetics.104.032193},
Key = {fds228323}
}
@article{fds228324,
Author = {Dong, X},
Title = {NPR1, all things considered.},
Journal = {Current opinion in plant biology},
Volume = {7},
Number = {5},
Pages = {547-552},
Year = {2004},
Month = {October},
ISSN = {1369-5266},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15337097},
Abstract = {Recent work has shown that the Arabidopsis NPR1 protein not
only plays an essential role in salicylic acid (SA)-mediated
systemic acquired resistance and rhizobacterium-triggered
induced systemic resistance, but also is involved in
crosstalk inhibition of jasmonic acid (JA)-mediated defense
responses. Molecular characterization has revealed that
activation of NPR1 and certain TGA transcription factors
occurs under the reducing conditions that follow an initial
oxidative burst after the induction of defense responses. In
addition to NPR1 and TGA, the single-stranded DNA-binding
transcription factor AtWhy1 and the WRKY70 transcription
factor were recently found to be involved in SA-mediated
defense and SA-JA crosstalk, respectively.},
Doi = {10.1016/j.pbi.2004.07.005},
Key = {fds228324}
}
@article{fds228291,
Author = {Dong, X},
Title = {The role of membrane-bound ankyrin-repeat protein ACD6 in
programmed cell death and plant defense.},
Journal = {Science's STKE : signal transduction knowledge
environment},
Volume = {2004},
Number = {221},
Pages = {pe6},
Year = {2004},
Month = {February},
url = {http://www.ncbi.nlm.nih.gov/pubmed/14983101},
Abstract = {Programmed cell death (PCD) is a common defense response in
plants against pathogen infection. The recently cloned ACD6
gene was identified in an Arabidopsis mutant, accelerated
cell death 6 (acd6), that undergoes PCD in the absence of a
pathogen challenge. ACD6 is a founding member of a large
family of genes that encode proteins with a short
amino-terminal region, nine ankyrin repeats in the middle,
and five putative transmembrane domains in the
carboxyl-terminal region. Characterization of the original
gain-of-function acd6 mutant and a transferred-DNA knockout
mutant acd6-T showed that ACD6 is an activator of the
defense pathway against bacterial pathogens and plays a role
in PCD through regulation of the defense signal salicylic
acid (SA). SA mediates not only downstream
pathogenesis-related (PR) genes, which encode proteins with
antimicrobial activities, but also ACD6, forming a feedback
signal amplification loop.},
Doi = {10.1126/stke.2212004pe6},
Key = {fds228291}
}
@article{fds228348,
Author = {Dong, X},
Title = {ACD6, an ankryn-repeat protein that both regulates and is
regulated by the plant hormone salicylic acid helps plants
defend against pathogens},
Journal = {Science's STKE},
Year = {2004},
Month = {February},
url = {http://www.stke.org/cgi/content/full/sigtrans;2004/221/pe6},
Key = {fds228348}
}
@article{fds228349,
Author = {Dong, X},
Title = {Pathogen-induced systemic DNA rearrangement in
plants.},
Journal = {Trends in plant science},
Volume = {9},
Number = {2},
Pages = {60-61},
Year = {2004},
Month = {February},
ISSN = {1360-1385},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15106587},
Abstract = {Infection of tobacco plants with tobacco mosaic virus and
oilseed rape mosaic virus was shown to induce a threefold
increase in homologous DNA recombination in non-infected
tissues. Grafting experiments by Igor Kovalchuk et al.
demonstrated that this increase was mediated by a systemic
recombination signal that traveled ahead of the virus. A
similar increase in DNA recombination was also observed in
the progeny of the infected plants, indicating that
pathogen-induced recombination can lead to heritable
adaptations to environmental stresses.},
Doi = {10.1016/j.tplants.2003.12.002},
Key = {fds228349}
}
@article{fds228307,
Author = {Durrant, WE and Dong, X},
Title = {Systemic acquired resistance.},
Journal = {Annual review of phytopathology},
Volume = {42},
Pages = {185-209},
Year = {2004},
Month = {January},
ISSN = {0066-4286},
url = {http://www.ncbi.nlm.nih.gov/pubmed/15283665},
Abstract = {Systemic acquired resistance (SAR) is a mechanism of induced
defense that confers long-lasting protection against a broad
spectrum of microorganisms. SAR requires the signal molecule
salicylic acid (SA) and is associated with accumulation of
pathogenesis-related proteins, which are thought to
contribute to resistance. Much progress has been made
recently in elucidating the mechanism of SAR. Using the
model plant Arabidopsis, it was discovered that the
isochorismate pathway is the major source of SA during SAR.
In response to SA, the positive regulator protein NPR1 moves
to the nucleus where it interacts with TGA transcription
factors to induce defense gene expression, thus activating
SAR. Exciting new data suggest that the mobile signal for
SAR might be a lipid molecule. We discuss the molecular and
genetic data that have contributed to our understanding of
SAR and present a model describing the sequence of events
leading from initial infection to the induction of defense
genes.},
Doi = {10.1146/annurev.phyto.42.040803.140421},
Key = {fds228307}
}
@article{fds228352,
Author = {Mou, Z and Fan, W and Dong, X},
Title = {Inducers of plant systemic acquired resistance regulate NPR1
function through redox changes.},
Journal = {Cell},
Volume = {113},
Number = {7},
Pages = {935-944},
Year = {2003},
Month = {June},
ISSN = {0092-8674},
url = {http://www.ncbi.nlm.nih.gov/pubmed/12837250},
Abstract = {NPR1 is an essential regulator of plant systemic acquired
resistance (SAR), which confers immunity to a broad-spectrum
of pathogens. SAR induction results in accumulation of the
signal molecule salicylic acid (SA), which induces defense
gene expression via activation of NPR1. We found that in an
uninduced state, NPR1 is present as an oligomer formed
through intermolecular disulfide bonds. Upon SAR induction,
a biphasic change in cellular reduction potential occurs,
resulting in reduction of NPR1 to a monomeric form.
Monomeric NPR1 accumulates in the nucleus and activates gene
expression. Inhibition of NPR1 reduction prevents defense
gene expression, whereas mutation of Cys82 or Cys216 in NPR1
leads to constitutive monomerization, nuclear localization
of the mutant proteins, and defense gene expression. These
data provide a missing link between accumulation of SA and
activation of NPR1 in the SAR signaling pathway.},
Doi = {10.1016/s0092-8674(03)00429-x},
Key = {fds228352}
}
@article{fds228353,
Author = {Spoel, SH and Koornneef, A and Claessens, SMC and Korzelius, JP and Van
Pelt, JA and Mueller, MJ and Buchala, AJ and Métraux, J-P and Brown, R and Kazan, K and Van Loon and LC and Dong, X and Pieterse,
CMJ},
Title = {NPR1 modulates cross-talk between salicylate- and
jasmonate-dependent defense pathways through a novel
function in the cytosol.},
Journal = {The Plant cell},
Volume = {15},
Number = {3},
Pages = {760-770},
Year = {2003},
Month = {March},
url = {http://dx.doi.org/10.1105/tpc.009159},
Abstract = {Plant defenses against pathogens and insects are regulated
differentially by cross-communicating signal transduction
pathways in which salicylic acid (SA) and jasmonic acid (JA)
play key roles. In this study, we investigated the molecular
mechanism of the antagonistic effect of SA on JA signaling.
Arabidopsis plants unable to accumulate SA produced 25-fold
higher levels of JA and showed enhanced expression of the
JA-responsive genes LOX2, PDF1.2, and VSP in response to
infection by Pseudomonas syringae pv tomato DC3000,
indicating that in wild-type plants, pathogen-induced SA
accumulation is associated with the suppression of JA
signaling. Analysis of the Arabidopsis mutant npr1, which is
impaired in SA signal transduction, revealed that the
antagonistic effect of SA on JA signaling requires the
regulatory protein NPR1. Nuclear localization of NPR1, which
is essential for SA-mediated defense gene expression, is not
required for the suppression of JA signaling, indicating
that cross-talk between SA and JA is modulated through a
novel function of NPR1 in the cytosol.},
Doi = {10.1105/tpc.009159},
Key = {fds228353}
}
@article{fds228351,
Author = {Zhang, Y and Dong, X and Li, X},
Title = {A gain-of-function mutation in a plant disease resistance
gene leads to constitutive activation of downstream signal
transduction pathways in the snc1 mutant},
Journal = {Plant Cell},
Volume = {15},
Number = {11},
Pages = {2636},
Year = {2003},
url = {http://dx.doi.org/10.1105/tpc.015842},
Abstract = {Plants have evolved sophisticated defense mechanisms against
pathogen infections, during which resistance (R) genes play
central roles in recognizing pathogens and initiating
defense cascades. Most of the cloned R genes share two
common domains: the central domain, which encodes a
nucleotide binding adaptor shared by APAF-1, certain R
proteins, and CED-4 (NB-ARC), plus a C-terminal region that
encodes Leu-rich repeats (LRR). In Arabidopsis, a dominant
mutant, suppressor of npr1-1, constitutive 1 (snc1), was
identified previously that constitutively expresses
pathogenesis-related (PR) genes and resistance against both
Pseudomonas syringae pv maculicola ES4326 and Peronospora
parasitica Noco2. The snc1 mutation was mapped to the RPP4
cluster. In snc1, one of the TIR-NB-LRR-type R genes
contains a point mutation that results in a single amino
acid change from Glu to Lys in the region between NB-ARC and
LRR. Deletions of this R gene in snc1 reverted the plants to
wild-type morphology and completely abolished constitutive
PR gene expression and disease resistance. The constitutive
activation of the defense responses was not the result of
the overexpression of the R gene, because its expression
level was not altered in snc1. Our data suggest that the
point mutation in snc1 renders the R gene constitutively
active without interaction with pathogens. To analyze signal
transduction pathways downstream of snc1, epistasis analyses
between snc1 and pad4-1 or eds5-3 were performed. Although
the resistance signaling in snc1 was fully dependent on
PAD4, it was only partially affected by blocking salicylic
acid (SA) synthesis, suggesting that snc1 activates both
SA-dependent and SA-independent resistance
pathways.},
Doi = {10.1105/tpc.015842},
Key = {fds228351}
}
@article{fds304258,
Author = {Fan, W and Dong, X},
Title = {In vivo interaction between NPR1 and transcription factor
TGA2 leads to salicylic acid-mediated gene activation in
Arabidopsis.},
Journal = {The Plant cell},
Volume = {14},
Number = {6},
Pages = {1377-1389},
Year = {2002},
Month = {June},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/12084833},
Abstract = {The Arabidopsis NPR1 protein is a key regulator of salicylic
acid (SA)-mediated gene expression in systemic acquired
resistance. Based on yeast two-hybrid analysis, NPR1 has
been suggested to interact with members of the TGA family of
transcription factors, including TGA2 (AHBP-1b). However,
genetic evidence demonstrating that the NPR1-TGA interaction
occurs in planta is still lacking, and the role of this
interaction in SA-mediated gene activation has yet to be
determined. In this study, we expressed a truncated form of
TGA2 in Arabidopsis and found that the resulting transgenic
lines displayed phenotypes similar to those of npr1 mutants.
This dominant-negative effect of the TGA2 mutant shows that
TGA2 and NPR1 interact in planta. We also present
biochemical evidence indicating that this interaction is
specific and enhanced by SA treatment. Moreover, using a
chimera reporter system, we found that a chimeric TGA2GAL4
transcription factor activated a UAS(GAL)::GUS reporter gene
in response to SA and that this activation was abolished in
the npr1 mutant. NPR1 is required for the DNA binding
activity of the transcription factor. These genetic data
clearly demonstrate that TGA2 is a SA-responsive and
NPR1-dependent transcription activator.},
Doi = {10.1105/tpc.001628},
Key = {fds304258}
}
@article{fds228354,
Author = {Fan, W and Dong, X},
Title = {In Vivo Interaction between NPR1 and transcription},
Journal = {Plant Cell},
Volume = {14},
Number = {6},
Pages = {1377},
Year = {2002},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/12084833},
Abstract = {The Arabidopsis NPR1 protein is a key regulator of salicylic
acid (SA)-mediated gene expression in systemic acquired
resistance. Based on yeast two-hybrid analysis, NPR1 has
been suggested to interact with members of the TGA family of
transcription factors, including TGA2 (AHBP-1b). However,
genetic evidence demonstrating that the NPR1-TGA interaction
occurs in planta is still lacking, and the role of this
interaction in SA-mediated gene activation has yet to be
determined. In this study, we expressed a truncated form of
TGA2 in Arabidopsis and found that the resulting transgenic
lines displayed phenotypes similar to those of npr1 mutants.
This dominant-negative effect of the TGA2 mutant shows that
TGA2 and NPR1 interact in planta. We also present
biochemical evidence indicating that this interaction is
specific and enhanced by SA treatment. Moreover, using a
chimera reporter system, we found that a chimeric TGA2GAL4
transcription factor activated a UAS(GAL)::GUS reporter gene
in response to SA and that this activation was abolished in
the npr1 mutant. NPR1 is required for the DNA binding
activity of the transcription factor. These genetic data
clearly demonstrate that TGA2 is a SA-responsive and
NPR1-dependent transcription activator.},
Key = {fds228354}
}
@article{fds228355,
Author = {Li, X and Clarke, JD and Zhang, Y and Dong, X},
Title = {Activation of an EDS1-mediated R-gene pathway in the snc1
mutant leads to constitutive, NPR1-independent pathogen
resistance.},
Journal = {Molecular plant-microbe interactions : MPMI},
Volume = {14},
Number = {10},
Pages = {1131-1139},
Year = {2001},
Month = {October},
ISSN = {0894-0282},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11605952},
Abstract = {The Arabidopsis NPR1 protein is an essential regulatory
component of systemic acquired resistance (SAR). Mutations
in the NPR1 gene completely block the induction of SAR by
signals such as salicylic acid (SA). An Arabidopsis mutant,
snc1 (suppressor of npr1-1, constitutive 1), was isolated in
a screen for suppressors of npr1-1. In the npr1-1
background, the snc1 mutation resulted in constitutive
resistance to Pseudomonas syringae maculicola ES4326 and
Peronospora parasitica Noco2. High levels of SA were
detected in the mutant and shown to be required for
manifestation of the snc1 phenotype. The snc1 mutation was
mapped to the RPP5 resistance (R) gene cluster and the eds1
mutation that blocks RPP5-mediated resistance suppressed
snc1. These data suggest that a RPP5-related resistance
pathway is activated constitutively in snc1. This pathway
does not employ NPR1 but requires the signal molecule SA and
the function of EDS1. Moreover, in snc1, constitutive
resistance is conferred in the absence of cell death, which
is often associated with R-gene mediated
resistance.},
Doi = {10.1094/mpmi.2001.14.10.1131},
Key = {fds228355}
}
@article{fds228346,
Author = {Dong, X},
Title = {Genetic dissection of systemic acquired resistance.},
Journal = {Current opinion in plant biology},
Volume = {4},
Number = {4},
Pages = {309-314},
Year = {2001},
Month = {August},
ISSN = {1369-5266},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11418340},
Abstract = {Significant progress has been made in the past year in
understanding the mechanism of systemic acquired resistance.
Mitogen-activated protein kinase cascades have been
implicated as negative regulators of salicyclic acid
accumulation and the induction of resistance. The salicylic
acid signal is transduced through NPR1, a nuclear-localized
protein that interacts with transcription factors that are
involved in regulating salicylic-acid-mediated gene
expression. Both promoter analyses and genetic studies have
shown that gene expression in systemic acquired resistance
requires not only the activation of a transcriptional
activator(s) but also inhibition of a transcriptional
repressor(s). Microarray experiments have been performed to
search for those genes whose expression is transcriptionally
regulated during systemic acquired resistance and to
identify common promoter elements that control these
genes.},
Doi = {10.1016/s1369-5266(00)00178-3},
Key = {fds228346}
}
@article{fds228344,
Author = {Chern, MS and Fitzgerald, HA and Yadav, RC and Canlas, PE and Dong, X and Ronald, PC},
Title = {Evidence for a disease-resistance pathway in rice similar to
the NPR1-mediated signaling pathway in Arabidopsis.},
Journal = {The Plant journal : for cell and molecular
biology},
Volume = {27},
Number = {2},
Pages = {101-113},
Year = {2001},
Month = {July},
ISSN = {0960-7412},
url = {http://dx.doi.org/10.1046/j.1365-313x.2001.01070.x},
Abstract = {The Arabidopsis NPR1/NIM1 gene is a key regulator of
systemic acquired resistance (SAR). Over-expression of NPR1
leads to enhanced resistance in Arabidopsis. To investigate
the role of NPR1 in monocots, we over-expressed the
Arabidopsis NPR1 in rice and challenged the transgenic
plants with Xanthomonas oryzae pv. oryzae (Xoo), the rice
bacterial blight pathogen. The transgenic plants displayed
enhanced resistance to Xoo. RNA blot hybridization indicates
that enhanced resistance requires expression of NPR1 mRNA
above a threshold level in rice. To identify components
mediating the resistance controlled by NPR1, we used NPR1 as
bait in a yeast two-hybrid screen. We isolated four cDNA
clones encoding rice NPR1 interactors (named rTGA2.1,
rTGA2.2, rTGA2.3 and rLG2) belonging to the bZIP family.
rTGA2.1, rTGA2.2 and rTGA2.3 share 75, 76 and 78% identity
with Arabidopsis TGA2, respectively. In contrast, rLG2
shares highest identity (81%) to the maize liguleless (LG2)
gene product, which is involved in establishing the leaf
blade-sheath boundary. The interaction of NPR1 with the rice
bZIP proteins in yeast was impaired by the npr1-1 and npr1-2
mutations, but not by the nim1-4 mutation. The NPR1-rTGA2.1
interaction was confirmed by an in vitro pull-down
experiment. In gel mobility shift assays, rTGA2.1 binds to
the rice RCH10 promoter and to a cis-element required
sequence-specifically for salicylic acid responsiveness.
This is the first demonstration that the Arabidopsis NPR1
gene can enhance disease resistance in a monocot plant.
These results also suggest that monocot and dicot plants
share a conserved signal transduction pathway controlling
NPR1-mediated resistance.},
Doi = {10.1046/j.1365-313x.2001.01070.x},
Key = {fds228344}
}
@article{fds228343,
Author = {Clarke, JD and Aarts, N and Feys, BJ and Dong, X and Parker,
JE},
Title = {Constitutive disease resistance requires EDS1 in the
Arabidopsis mutants cpr1 and cpr6 and is partially
EDS1-dependent in cpr5.},
Journal = {The Plant journal : for cell and molecular
biology},
Volume = {26},
Number = {4},
Pages = {409-420},
Year = {2001},
Month = {May},
ISSN = {0960-7412},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11439128},
Abstract = {The systemic acquired resistance (SAR) response in
Arabidopsis is characterized by the accumulation of
salicylic acid (SA), expression of the pathogenesis-related
(PR) genes, and enhanced resistance to virulent bacterial
and oomycete pathogens. The cpr (constitutive expressor of
PR genes) mutants express all three SAR phenotypes. In
addition, cpr5 and cpr6 induce expression of PDF1.2, a
defense-related gene associated with activation of the
jasmonate/ethylene-mediated resistance pathways. cpr5 also
forms spontaneous lesions. In contrast, the eds1 (enhanced
disease susceptibility) mutation abolishes race-specific
resistance conferred by a major subclass of resistance (R)
gene products in response to avirulent pathogens. eds1
plants also exhibit increased susceptibility to virulent
pathogens. Epistasis experiments were designed to explore
the relationship between the cpr- and EDS1-mediated
resistance pathways. We found that a null eds1 mutation
suppresses the disease resistance phenotypes of both cpr1
and cpr6. In contrast, eds1 only partially suppresses
resistance in cpr5, leading us to conclude that cpr5
expresses both EDS1-dependent and EDS1-independent
components of plant disease resistance. Although eds1 does
not prevent lesion formation on cpr5 leaves, it alters their
appearance and reduces their spread. This phenotypic
difference is associated with increased pathogen
colonization of cpr5 eds1 plants compared to cpr5. The data
allow us to place EDS1 as a necessary downstream component
of cpr1- and cpr6-mediated responses, but suggest a more
complex relationship between EDS1 and cpr5 in plant
defense.},
Doi = {10.1046/j.1365-313x.2001.2641041.x},
Key = {fds228343}
}
@article{fds228345,
Author = {Jirage, D and Zhou, N and Cooper, B and Clarke, JD and Dong, X and Glazebrook, J},
Title = {Constitutive salicylic acid-dependent signaling in cpr1 and
cpr6 mutants requires PAD4.},
Journal = {The Plant journal : for cell and molecular
biology},
Volume = {26},
Number = {4},
Pages = {395-407},
Year = {2001},
Month = {May},
ISSN = {0960-7412},
url = {http://dx.doi.org/10.1046/j.1365-313x.2001.2641040.x},
Abstract = {Salicylic acid (SA)-dependent signaling controls activation
of a set of plant defense mechanisms that are important for
resistance to a variety of microbial pathogens. Many
Arabidopsis mutants that display altered SA-dependent
signaling have been isolated. We used double mutant analysis
to determine the relative positions of the pad4, cpr1, cpr5,
cpr6, dnd1 and dnd2 mutations in the signal transduction
network leading to SA-dependent activation of defense gene
expression and disease resistance. The pad4 mutation causes
failure of SA accumulation in response to infection by
certain pathogens, while the other mutations cause
constitutively high levels of SA, defense gene expression
and resistance. The cpr1 pad4, cpr5 pad4, cpr6 pad4, dnd1
pad4 and dnd2 pad4 double mutants were constructed and
assayed for stature, presence of spontaneous lesions,
resistance to Pseudomonas syringae and Peronospora
parasitica, SA levels, expression of PAD4, PR-1 and PDF1.2,
and accumulation of camalexin. We found that the effects of
the cpr1 and cpr6 mutations on SA-dependent gene expression
are completely dependent on PAD4 function. In contrast, SA
accumulation in the lesion-mimic mutant cpr5 is partially
PAD4-independent, while in dnd1 and dnd2 mutants it is
completely PAD4-independent. A model describing a possible
arrangement of activities in the signal transduction network
is presented.},
Doi = {10.1046/j.1365-313x.2001.2641040.x},
Key = {fds228345}
}
@article{fds228289,
Author = {Dong, X and Li, X and Zhang, Y and Fan, W and Kinkema, M and Clarke,
J},
Title = {Regulation of systemic acquired resistance by NPR1 and its
partners.},
Journal = {Novartis Foundation symposium},
Volume = {236},
Pages = {165-173},
Year = {2001},
Month = {January},
ISSN = {1528-2511},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11387978},
Abstract = {The NPR1 protein of Arabidopsis thaliana has been shown to
be an important regulatory component of systemic acquired
resistance (SAR). Mutations in the NPR1 gene block the
induction of SAR by the signal molecule salicylic acid (SA).
NPR1 contains an ankyrin repeats and a BTB domain which are
involved in interaction with other protein(s). To further
study the function of NPR1 and the regulatory mechanism of
SAR, we used both molecular and genetic approaches to
identify additional SAR regulatory components. Through a
yeast two-hybrid screen we found that NPR1 interacts
specifically with bZIP transcription factors. The
involvement of bZIP transcription factors in controlling the
SA-induced genes had been suggested by a number of promoter
studies performed on these genes. It was found that as1
element, which is a binding site for bZIP transcription
factors, is essential for SA-induced gene expression. In a
genetic screen for suppressors of npr1, we found a mutant,
sni1, that restored the responsiveness to SAR induction in
npr1. The genetic characteristics of the sni1 mutant and the
sequence of SNI1 suggest that the wild-type SNI1 protein is
a negative regulator of SAR. We believe that SAR is
controlled by both positive regulators and negative
regulators.},
Doi = {10.1002/9780470515778.ch12},
Key = {fds228289}
}
@article{fds228288,
Author = {Dong, X and Braun, EL and Grotewold, E},
Title = {Functional conservation of plant secondary metabolic enzymes
revealed by complementation of Arabidopsis flavonoid mutants
with maize genes},
Journal = {Plant Physiology},
Volume = {127},
Number = {1},
Pages = {46-57},
Year = {2001},
url = {http://dx.doi.org/10.1104/pp.127.1.46},
Abstract = {Mutations in the transparent testa (tt) loci abolish pigment
production in Arabidopsis seed coats. The TT4, TT5, and TT3
loci encode chalcone synthase, chalcone isomerase, and
dihydroflavonol 4-reductase, respectively, which are
essential for anthocyanin accumulation and may form a
macromolecular complex. Here, we show that the products of
the maize (Zea mays) C2, CHI1, and A1 genes complement
Arabidopsis tt4, tt5, and tt3 mutants, restoring the ability
of these mutants to accumulate pigments in seed coats and
seedlings. Overexpression of the maize genes in wild-type
Arabidopsis seedlings does not result in increased
anthocyanin accumulation, suggesting that the steps
catalyzed by these enzymes are not rate limiting in the
conditions assayed. The expression of the maize A1 gene in
the flavonoid 3′ hydroxylase Arabidopsis tt7 mutant
resulted in an increased accumulation of pelargonidin. We
conclude that enzymes involved in secondary metabolism can
be functionally exchangeable between plants separated by
large evolutionary distances. This is in sharp contrast to
the notion that the more relaxed selective constrains to
which secondary metabolic pathways are subjected is
responsible for the rapid divergence of the corresponding
enzymes.},
Doi = {10.1104/pp.127.1.46},
Key = {fds228288}
}
@article{fds228342,
Author = {Li, X and Song, Y and Century, K and Straight, S and Ronald, P and Dong, X and Lassner, M and Zhang, Y},
Title = {A fast neutron deletion mutagenesis-based reverse genetics
system for plants},
Journal = {Plant J.},
Volume = {27},
Number = {3},
Pages = {235-242},
Year = {2001},
ISSN = {0960-7412},
url = {http://dx.doi.org/10.1046/j.1365-313x.2001.01084.x},
Abstract = {A new reverse genetics method has been developed to identify
and isolate deletion mutants for targeted plant genes.
Deletion mutant libraries are generated using fast neutron
bombardment. DNA samples extracted from the deletion
libraries are used to screen for deletion mutants by
polymerase chain reaction (PCR) using specific primers
flanking the targeted genes. By adjusting PCR conditions to
preferentially amplify the deletion alleles, deletion
mutants were identified in pools of DNA samples, each pool
containing DNA from 2592 mutant lines. Deletion mutants were
obtained for 84% of targeted loci from an Arabidopsis
population of 51 840 lines. Using a similar approach, a
deletion mutant for a rice gene was identified. Thus we
demonstrate that it is possible to apply this method to
plant species other than Arabidopsis. As fast neutron
mutagenesis is highly efficient, it is practical to develop
deletion mutant populations with more complete coverage of
the genome than obtained with methods based on insertional
mutagenesis. Because fast neutron mutagenesis is applicable
to all plant genetic systems, this method has the potential
to enable reverse genetics for a wide range of plant
species.},
Doi = {10.1046/j.1365-313x.2001.01084.x},
Key = {fds228342}
}
@article{fds228341,
Author = {Kinkema, M and Fan, W and Dong, X},
Title = {Nuclear localization of NPR1 is required for activation of
PR gene expression.},
Journal = {The Plant cell},
Volume = {12},
Number = {12},
Pages = {2339-2350},
Year = {2000},
Month = {December},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11148282},
Abstract = {Systemic acquired resistance (SAR) is a broad-spectrum
resistance in plants that involves the upregulation of a
battery of pathogenesis-related (PR) genes. NPR1 is a key
regulator in the signal transduction pathway that leads to
SAR. Mutations in NPR1 result in a failure to induce PR
genes in systemic tissues and a heightened susceptibility to
pathogen infection, whereas overexpression of the NPR1
protein leads to increased induction of the PR genes and
enhanced disease resistance. We analyzed the subcellular
localization of NPR1 to gain insight into the mechanism by
which this protein regulates SAR. An NPR1-green fluorescent
protein fusion protein, which functions the same as the
endogenous NPR1 protein, was shown to accumulate in the
nucleus in response to activators of SAR. To control the
nuclear transport of NPR1, we made a fusion of NPR1 with the
glucocorticoid receptor hormone binding domain. Using this
steroid-inducible system, we clearly demonstrate that
nuclear localization of NPR1 is essential for its activity
in inducing PR genes.},
Doi = {10.1105/tpc.12.12.2339},
Key = {fds228341}
}
@article{fds228340,
Author = {Clarke, JD and Volko, SM and Ledford, H and Ausubel, FM and Dong,
X},
Title = {Roles of salicylic acid, jasmonic acid, and ethylene in
cpr-induced resistance in arabidopsis.},
Journal = {The Plant cell},
Volume = {12},
Number = {11},
Pages = {2175-2190},
Year = {2000},
Month = {November},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11090217},
Abstract = {Disease resistance in Arabidopsis is regulated by multiple
signal transduction pathways in which salicylic acid (SA),
jasmonic acid (JA), and ethylene (ET) function as key
signaling molecules. Epistasis analyses were performed
between mutants that disrupt these pathways (npr1, eds5,
ein2, and jar1) and mutants that constitutively activate
these pathways (cpr1, cpr5, and cpr6), allowing exploration
of the relationship between the SA- and JA/ET-mediated
resistance responses. Two important findings were made.
First, the constitutive disease resistance exhibited by
cpr1, cpr5, and cpr6 is completely suppressed by the
SA-deficient eds5 mutant but is only partially affected by
the SA-insensitive npr1 mutant. Moreover, eds5 suppresses
the SA-accumulating phenotype of the cpr mutants, whereas
npr1 enhances it. These data indicate the existence of an
SA-mediated, NPR1-independent resistance response. Second,
the ET-insensitive mutation ein2 and the JA-insensitive
mutation jar1 suppress the NPR1-independent resistance
response exhibited by cpr5 and cpr6. Furthermore, ein2
potentiates SA accumulation in cpr5 and cpr5 npr1 while
dampening SA accumulation in cpr6 and cpr6 npr1. These
latter results indicate that cpr5 and cpr6 regulate
resistance through distinct pathways and that SA-mediated,
NPR1-independent resistance works in combination with
components of the JA/ET-mediated response
pathways.},
Doi = {10.1105/tpc.12.11.2175},
Key = {fds228340}
}
@article{fds350987,
Author = {Li, X and Zhang, YL and Clarke, J and Kinkema, M and Fan, WH and Dong,
XN},
Title = {Systemic acquired resistance is controlled by both positive
and negative regulators},
Journal = {BIOLOGY OF PLANT-MICROBE INTERACTIONS, VOL
2},
Pages = {282-286},
Publisher = {INTERNATIONAL SOC MOLECULAR PLANT-MICROBE
INTERACTIONS},
Editor = {DeWit, JGM and Bisseling, T and Stiekema, WJ},
Year = {2000},
Month = {January},
ISBN = {0-9654625-1-X},
Key = {fds350987}
}
@article{fds228356,
Author = {Zhang, Y and Fan, W and Kinkema, M and Li, X and Dong,
X},
Title = {Interaction of NPR1 with basic leucine zipper protein
transcription factors that bind sequences required for
salicylic acid induction of the PR-1 gene.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {96},
Number = {11},
Pages = {6523-6528},
Year = {1999},
Month = {May},
ISSN = {0027-8424},
url = {http://www.ncbi.nlm.nih.gov/pubmed/10339621},
Abstract = {The Arabidopsis thaliana NPR1 has been shown to be a key
regulator of gene expression during the onset of a plant
disease-resistance response known as systemic acquired
resistance. The npr1 mutant plants fail to respond to
systemic acquired resistance-inducing signals such as
salicylic acid (SA), or express SA-induced
pathogenesis-related (PR) genes. Using NPR1 as bait in a
yeast two-hybrid screen, we identified a subclass of
transcription factors in the basic leucine zipper protein
family (AHBP-1b and TGA6) and showed that they interact
specifically in yeast and in vitro with NPR1. Point
mutations that abolish the NPR1 function in A. thaliana also
impair the interactions between NPR1 and the transcription
factors in the yeast two-hybrid assay. Furthermore, a gel
mobility shift assay showed that the purified transcription
factor protein, AHBP-1b, binds specifically to an
SA-responsive promoter element of the A. thaliana PR-1 gene.
These data suggest that NPR1 may regulate PR-1 gene
expression by interacting with a subclass of basic leucine
zipper protein transcription factors.},
Doi = {10.1073/pnas.96.11.6523},
Key = {fds228356}
}
@article{fds228350,
Author = {Li, X and Zhang, Y and Clarke, JD and Li, Y and Dong,
X},
Title = {Identification and cloning of a negative regulator of
systemic acquired resistance, SNI1, through a screen for
suppressors of npr1-1},
Journal = {Cell},
Volume = {98},
Number = {3},
Pages = {329},
Year = {1999},
ISSN = {0092-8674},
url = {http://www.ncbi.nlm.nih.gov/pubmed/10458608},
Abstract = {Systemic acquired resistance (SAR) is a plant immune
response induced after a local infection by necrotizing
pathogens. The Arabidopsis NPR1 gene is a positive regulator
of SAR, essential for transducing the SAR signal salicylic
acid (SA). Mutations in the NPR1 gene abolish the SA-induced
expression of pathogenesis-related (PR) genes and resistance
to pathogens. To identify additional regulators of SAR, we
screened for suppressors of npr1-1. In the npr1-1
background, the sni1 (suppressor of npr1-1, inducible 1)
mutant shows near wild-type levels of PR1 expression and
resistance to pathogens after induction. Restoration of SAR
in npr1-1 by the recessive sni1 mutation indicates that
wild-type SNI1 may function as a negative regulator of SAR.
We cloned the SNI1 gene and found that it encodes a
leucine-rich nuclear protein.},
Doi = {10.1016/s0092-8674(00)81962-5},
Key = {fds228350}
}
@article{fds228325,
Author = {Dong, X},
Title = {SA, JA, ethylene, and disease resistance in
plants.},
Journal = {Current opinion in plant biology},
Volume = {1},
Number = {4},
Pages = {316-323},
Year = {1998},
Month = {August},
ISSN = {1369-5266},
url = {http://www.ncbi.nlm.nih.gov/pubmed/10066607},
Abstract = {Exciting advances have been made during the past year:
isolating mutants affecting plant disease resistance,
cloning genes involved in the regulation of various defense
responses, and characterizing novel defense signaling
pathways. Recent studies have demonstrated that jasmonic
acid and ethylene are important for the induction of
nonspecific disease resistance through signaling pathways
that are distinct from the classical systemic acquired
resistance response pathway regulated by salicylic
acid.},
Doi = {10.1016/1369-5266(88)80053-0},
Key = {fds228325}
}
@article{fds228327,
Author = {Cao, H and Li, X and Dong, X},
Title = {Generation of broad-spectrum disease resistance by
overexpression of an essential regulatory gene in systemic
acquired resistance.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {95},
Number = {11},
Pages = {6531-6536},
Year = {1998},
Month = {May},
ISSN = {0027-8424},
url = {http://www.ncbi.nlm.nih.gov/pubmed/9601001},
Abstract = {The recently cloned NPR1 gene of Arabidopsis thaliana is a
key regulator of acquired resistance responses. Upon
induction, NPR1 expression is elevated and the NPR1 protein
is activated, in turn inducing expression of a battery of
downstream pathogenesis-related genes. In this study, we
found that NPR1 confers resistance to the pathogens
Pseudomonas syringae and Peronospora parasitica in a
dosage-dependent fashion. Overexpression of NPR1 leads to
enhanced resistance with no obvious detrimental effect on
the plants. Thus, for the first time, a single gene is shown
to be a workable target for genetic engineering of
nonspecific resistance in plants.},
Doi = {10.1073/pnas.95.11.6531},
Key = {fds228327}
}
@article{fds228326,
Author = {Clarke, JD and Liu, Y and Klessig, DF and Dong, X},
Title = {Uncoupling PR-gene expression from NPR1 and bacterial
resistance: Characterization of the dominant Arabidopsis
cpr6 mutant.},
Journal = {Plant Cell},
Volume = {10},
Number = {4},
Pages = {557-567},
Year = {1998},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/9548982},
Abstract = {In Arabidopsis, NPR1 mediates the salicylic acid
(SA)-induced expression of pathogenesis-related (PR) genes
and systemic acquired resistance (SAR). Here, we report the
identification of another component, CPR 6, that may
function with NPR1 in regulating PR gene expression. The
dominant CPR 6-1 mutant expresses the SA/NPR1-regulated PR
genes (PR-1, BGL 2, and PR-5) and displays enhanced
resistance to Pseudomonas syringae pv maculicola ES4326 and
Peronospora parasitica Noco2 in the absence of SAR
induction. cpr 6-1-induced PR gene expression is not
suppressed in the cpr 6-1 npr1-1 double mutant but is
suppressed when SA is removed by salicylate hydroxylase.
Thus, constitutive PR gene expression in cpr 6-1 requires SA
but not NPR1. In addition, resistance to P. s. maculicola
ES4326 is suppressed in the cpr 6-1 npr1-1 double mutant,
despite expression of PR-1, BGL 2, and PR-5. Resistance to
P. s. maculicola ES4326 must therefore be accomplished
through unidentified antibacterial gene products that are
regulated through NPR1. These results show that CPR 6 is an
important regulator of multiple signal transduction pathways
involved in plant defense.},
Doi = {10.1105/tpc.10.4.557},
Key = {fds228326}
}
@article{fds228329,
Author = {Cao, H and Glazebrook, J and Clarke, JD and Volko, S and Dong,
X},
Title = {The Arabidopsis NPR1 gene that controls systemic acquired
resistance encodes a novel protein containing ankyrin
repeats.},
Journal = {Cell},
Volume = {88},
Number = {1},
Pages = {57-63},
Year = {1997},
Month = {January},
ISSN = {0092-8674},
url = {http://www.ncbi.nlm.nih.gov/pubmed/9019406},
Abstract = {The Arabidopsis NPR1 gene controls the onset of systemic
acquired resistance (SAR), a plant immunity, to a broad
spectrum of pathogens that is normally established after a
primary exposure to avirulent pathogens. Mutants with
defects in NPR1 fail to respond to various SAR-inducing
treatments, displaying little expression of
pathogenesis-related (PR) genes and exhibiting increased
susceptibility to infections. NPR1 was cloned using a
map-based approach and was found to encode a novel protein
containing ankyrin repeats. The lesion in one npr1 mutant
allele disrupted the ankyrin consensus sequence, suggesting
that these repeats are important for NPR1 function.
Furthermore, transformation of the cloned wild-type NPR1
gene into npr1 mutants not only complemented the mutations,
restoring the responsiveness to SAR induction with respect
to PR-gene expression and resistance to infections, but also
rendered the transgenic plants more resistant to infection
by P. syringae in the absence of SAR induction.},
Doi = {10.1016/s0092-8674(00)81858-9},
Key = {fds228329}
}
@article{fds228328,
Author = {Bowling, SA and Clarke, JD and Liu, Y and Klessig, DF and Dong,
X},
Title = {The cpr5 mutant of Arabidopsis expresses both NPR1-dependent
and NPR1-independent resistance.},
Journal = {Plant Cell},
Volume = {9},
Number = {9},
Pages = {1573-1584},
Year = {1997},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/9338960},
Abstract = {The cpr5 mutant was identified from a screen for
constitutive expression of systemic acquired resistance
(SAR). This single recessive mutation also leads to
spontaneous expression of chlorotic lesions and reduced
trichome development. The cpr5 plants were found to be
constitutively resistant to two virulent pathogens,
Pseudomonas syringae pv maculicola ES4326 and Peronospora
parasitica Noco2; to have endogenous expression of the
pathogenesis-related gene 1 (PR-1); and to have an elevated
level of salicylic acid (SA). Lines homozygous for cpr5 and
either the SA-degrading bacterial gene nahG or the
SA-insensitive mutation npr1 do not express PR-1 or exhibit
resistance to P. s. maculicola ES4326. Therefore, we
conclude that cpr5 acts upstream of SA in inducing SAR.
However, the cpr5 npr1 plants retained heightened resistance
to P. parasitica Noco2 and elevated expression of the
defensin gene PDF1.2, implying that NPR1-independent
resistance signaling also occurs. We conclude that the cpr5
mutation leads to constitutive expression of both an
NPR1-dependent and an NPR1-independent SAR pathway.
Identification of this mutation indicates that these
pathways are connected in early signal transduction steps
and that they have overlapping functions in providing
resistance.},
Doi = {10.1105/tpc.9.9.1573},
Key = {fds228328}
}
@article{fds228330,
Author = {Dong, X},
Title = {Finding the missing pieces in the puzzle of plant disease
resistance.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {92},
Number = {16},
Pages = {7137-7139},
Year = {1995},
Month = {August},
ISSN = {0027-8424},
url = {http://www.ncbi.nlm.nih.gov/pubmed/11607565},
Doi = {10.1073/pnas.92.16.7137},
Key = {fds228330}
}
@article{fds327322,
Author = {DONG, X and BOWLING, SA and CAO, H},
Title = {GENETIC DISSECTION OF THE SAR SIGNAL-TRANSDUCTION PATHWAY(S)
IN ARABIDOPSIS},
Journal = {JOURNAL OF CELLULAR BIOCHEMISTRY},
Pages = {486-486},
Publisher = {WILEY-LISS},
Year = {1995},
Month = {March},
Key = {fds327322}
}
@article{fds228331,
Author = {Bowling, SA and Guo, A and Cao, H and Gordon, AS and Klessig, DF and Dong,
X},
Title = {A mutation in Arabidopsis that leads to constitutive
expression of systemic acquired resistance.},
Journal = {The Plant cell},
Volume = {6},
Number = {12},
Pages = {1845-1857},
Year = {1994},
Month = {December},
ISSN = {1040-4651},
url = {http://www.ncbi.nlm.nih.gov/pubmed/7866028},
Abstract = {Systemic acquired resistance (SAR) is a nonspecific defense
response in plants that is associated with an increase in
the endogenous level of salicylic acid (SA) and elevated
expression of pathogenesis-related (PR) genes. To identify
mutants involved in the regulation of PR genes and the onset
of SAR, we transformed Arabidopsis with a reporter gene
containing the promoter of a beta-1,3-glucanase-encoding PR
gene (BGL2) and the coding region of beta-glucuronidase
(GUS). The resulting transgenic line (BGL2-GUS) was
mutagenized, and the M2 progeny were scored for constitutive
GUS activity. We report the characterization of one mutant,
cpr1 (constitutive expressor of PR genes), that was
identified in this screen and shown by RNA gel blot analysis
also to have elevated expression of the endogenous PR genes
BGL2, PR-1, and PR-5. Genetic analyses indicated that the
phenotype conferred by cpr1 is caused by a single, recessive
nuclear mutation and is suppressed in plants producing a
bacterial salicylate hydroxylase, which inactivates SA.
Furthermore, biochemical analysis showed that the endogenous
level of SA is elevated in the mutant. Finally, the cpr1
plants were found to be resistant to the fungal pathogen
Peronospora parasitica NOCO2 and the bacterial pathogen
Pseudomonas syringae pv maculicola ES4326, which are
virulent in wild-type BGL2-GUS plants. Because the cpr1
mutation is recessive and associated with an elevated
endogenous level of SA, we propose that the CPR1 gene
product acts upstream of SA as a negative regulator of
SAR.},
Doi = {10.1105/tpc.6.12.1845},
Key = {fds228331}
}
@article{fds228332,
Author = {Cao, H and Bowling, SA and Gordon, AS and Dong, X},
Title = {Characterization of an Arabidopsis Mutant That Is
Nonresponsive to Inducers of Systemic Acquired
Resistance.},
Journal = {The Plant cell},
Volume = {6},
Number = {11},
Pages = {1583-1592},
Year = {1994},
Month = {November},
url = {http://www.ncbi.nlm.nih.gov/pubmed/12244227},
Abstract = {Systemic acquired resistance (SAR) is a general defense
response in plants that is characterized by the expression
of pathogenesis-related (PR) genes. SAR can be induced after
a hypersensitive response to an avirulent pathogen or by
treatment with either salicylic acid (SA) or
2,6-dichloroisonicotinic acid (INA). To dissect the signal
transduction pathway of SAR, we isolated an Arabidopsis
mutant that lacks the expression of an SA-, INA-, and
pathogen-responsive chimeric reporter gene composed of the
5[prime] untranslated region of an Arabidopsis PR gene,
[beta]-1,3-glucanase (BGL2), and the coding region of
[beta]-glucuronidase (GUS). This mutant, npr1 (nonexpresser
of PR genes), carries a single recessive mutation that
abolishes the SAR-responsive expression of other PR genes as
well. While SA-, INA-, or avirulent pathogen-induced SAR
protects wild-type plants from Pseudomonas syringae
infection, the mutant cannot be protected by pretreatment
with these inducers. The insensitivity of npr1 to SA, INA,
and avirulent pathogens in SAR induction indicates that
these inducers share a common signal transduction pathway.
Moreover, in npr1, the localized expression of PR genes
induced by a virulent Pseudomonas pathogen is disrupted, and
the lesion formed is less confined. These results suggest a
role for PR genes in preventing the proximal spread of
pathogens in addition to their suggested role in
SAR.},
Doi = {10.1105/tpc.6.11.1583},
Key = {fds228332}
}
@article{fds228334,
Author = {Melan, MA and Dong, X and Endara, ME and Davis, KR and Ausubel, FM and Peterman, TK},
Title = {An Arabidopsis thaliana lipoxygenase gene can be induced by
pathogens, abscisic acid, and methyl jasmonate.},
Journal = {Plant physiology},
Volume = {101},
Number = {2},
Pages = {441-450},
Year = {1993},
Month = {February},
url = {http://dx.doi.org/10.1104/pp.101.2.441},
Abstract = {We isolated and characterized a 2.8-kb, full-length,
Arabidopsis thaliana cDNA clone encoding a lipoxygenase. DNA
sequence analysis showed that the deduced amino acid
sequence of the Arabidopsis protein is 72 to 78% similar to
that of legume seed lipoxygenases. DNA blot analysis
indicated that Arabidopsis contains a single gene, LOX1,
with appreciable homology to the cDNA clone. RNA blot
analysis showed that the LOX1 gene is expressed in
Arabidopsis leaves, roots, inflorescences, and young
seedlings. LOX1 expression levels were highest in roots and
young seedlings. In mature plants, LOX1 mRNA levels
increased upon treatment with the stress-related hormones
abscisic acid and methyl jasmonate and remained high for at
least 96 h. Expression of the LOX1 gene was examined
following infiltration of leaves with virulent (Psm ES4326)
and avirulent (Pst MM1065) strains of Pseudomonas syringae.
LOX1 mRNA levels were induced approximately 6-fold by both
virulent and avirulent strains; however, the response to
avirulent strains was much more rapid. Infiltration of
leaves with Pst MM1065 resulted in maximal induction within
12 h, whereas maximal induction by Psm ES4326 did not occur
until 48 h. When a cloned avr gene, avrRpt2, was transferred
to Psm ES4326, LOX1 mRNA accumulated in a pattern similar to
that observed for the avirulent strain Pst
MM1065.},
Doi = {10.1104/pp.101.2.441},
Key = {fds228334}
}
@article{fds228333,
Author = {Keith, B and Dong, XN and Ausubel, FM and Fink, GR},
Title = {Differential induction of 3-deoxy-D-arabino-heptulosonate
7-phosphate synthase genes in Arabidopsis thaliana by
wounding and pathogenic attack.},
Journal = {Proceedings of the National Academy of Sciences of the
United States of America},
Volume = {88},
Number = {19},
Pages = {8821-8825},
Year = {1991},
Month = {October},
url = {http://dx.doi.org/10.1073/pnas.88.19.8821},
Abstract = {We have isolated cDNAs from two distinct genes encoding
3-deoxy-D-arabino-heptulosonate 7-phosphate (DAHP) synthase
(EC 4.1.2.15) in Arabidopsis thaliana. Predicted protein
sequences from both genes, DHS1 and DHS2, and a potato DAHP
synthase gene are highly related, but none shows significant
sequence similarity to conserved microbial DAHP synthase
proteins. Despite this structural difference, the DHS1 cDNA
complements mutations in a yeast strain lacking DAHP
synthase activity. DHS1 RNA levels increase in Arabidopsis
leaves subjected either to physical wounding or to
infiltration with pathogenic Pseudomonas syringae strains.
DHS2 RNA levels are not increased by these treatments,
suggesting that the DHS1 and DHS2 proteins fulfill different
physiological functions. Other enzymes in the Arabidopsis
aromatic pathway are also encoded by duplicated genes, an
arrangement that may allow independent regulation of
aromatic amino acid biosynthesis by distinct physiological
requirements such as protein synthesis and secondary
metabolism. The presence of amino-terminal extensions
characteristic of chloroplast transit peptides on DHS1 and
DHS2 suggests that both proteins may be targeted to the
chloroplast.},
Doi = {10.1073/pnas.88.19.8821},
Key = {fds228333}
}
@article{fds228335,
Author = {Dong, X and Mindrinos, M and Davis, KR and Ausubel,
FM},
Title = {Induction of Arabidopsis defense genes by virulent and
avirulent Pseudomonas syringae strains and by a cloned
avirulence gene.},
Journal = {The Plant cell},
Volume = {3},
Number = {1},
Pages = {61-72},
Year = {1991},
Month = {January},
url = {http://dx.doi.org/10.1105/tpc.3.1.61},
Abstract = {We developed a model system to study the signal transduction
pathways leading to the activation of Arabidopsis thaliana
genes involved in the defense against pathogen attack. Here
we describe the identification and characterization of
virulent and avirulent Pseudomonas syringae strains that
elicit disease or resistance symptoms when infiltrated into
Arabidopsis leaves. The virulent and avirulent strains were
characterized by determining growth of the pathogen in
Arabidopsis leaves and by measuring accumulation of mRNA
corresponding to Arabidopsis phenylalanine ammonia-lyase
(PAL), beta-1,3-glucanase (BG), and chalcone synthase (CHS)
genes in infected leaves. The virulent strain, P. syringae
pv maculicola ES4326, multiplied 10(5)-fold in Arabidopsis
leaves and strongly elicited BG1, BG2, and BG3 mRNA
accumulation but had only a modest effect on PAL mRNA
accumulation. In contrast, the avirulent strain, P. syringae
pv tomato MM1065, multiplied less than 10-fold in leaves and
had only a minimal effect on BG1, BG2, and BG3 mRNA
accumulation, but it induced PAL mRNA accumulation. No
accumulation of CHS mRNA was found with either ES4326 or
MM1065. We also describe the cloning of a putative
avirulence (avr) gene from the avirulent strain MM1065 that
caused the virulent strain ES4326 to grow less well in
leaves and to strongly elicit PAL but not BG1 and BG3 mRNA
accumulation. These results suggest that the Arabidopsis PAL
and BG genes may be activated by distinct signal
transduction pathways and show that differences in plant
gene induction by virulent and avirulent strains can be
attributed to a cloned presumptive avr gene.},
Doi = {10.1105/tpc.3.1.61},
Key = {fds228335}
}
@article{fds20975,
Author = {Schott, E. J. and K.R. Davis and X. Dong and M. Mindrinos P. Guevara and F.M. Ausubel.},
Title = {Pseudomonas syringae infection of Arabidopsis thaliana as a
model system for studying plant-bacterial
interactions.},
Journal = {In Pseudomonas: Biotransformation, Pathogenesis, and
Evolving Biotechnology. S. Silver, A.M. Chakrabarty. B.
Iglewski, and S. Kaplan, eds.},
Pages = {82-90},
Year = {1990},
Key = {fds20975}
}
@article{fds228336,
Author = {Dong, XN and Rouillard, KP and Womble, DD and Rownd,
RH},
Title = {DNA bending near the replication origin of IncFII plasmid
NR1.},
Journal = {Journal of bacteriology},
Volume = {171},
Number = {2},
Pages = {703-707},
Year = {1989},
Month = {February},
url = {http://dx.doi.org/10.1128/jb.171.2.703-707.1989},
Abstract = {The DNA replication origin of plasmid NR1 is located
approximately 190 base pairs downstream from the 3' end of
the repA1 gene, which encodes the essential initiation
protein for replication of the plasmid. Restriction
endonuclease fragments that contain the NR1 replication
origin and its flanking sequences at circularly permuted
positions were obtained by digesting oligomers of
ori-containing DNA fragments with sets of enzymes that each
cut only once in every ori fragment. Polyacrylamide gel
electrophoresis of these permuted restriction fragments
showed anomalous mobilities, indicating the presence of a
DNA bending locus. Through analysis of the relative mobility
plots of these permuted fragments, we found one or two
possible DNA bending sites located in the intervening region
between the repA1 gene and the replication origin of NR1. It
seems possible that DNA bending in this region might help to
orient the replication origin alongside the repA1 gene,
which could contribute to the cis-acting character of the
RepA1 initiation protein.},
Doi = {10.1128/jb.171.2.703-707.1989},
Key = {fds228336}
}
@article{fds20974,
Author = {Davis, K. R. and E. Schott and X. Dong and F. M.
Ausubel},
Title = {Arabidopsis thaliana as a model system for studying
plant-pathogen interactions.},
Journal = {In Signal molecules in plants and plant-microbe interaction.
B. J. J. Lugtenberg, ed.},
Pages = {99-106},
Year = {1989},
Key = {fds20974}
}
@article{fds228337,
Author = {Dong, XN and Womble, DD and Rownd, RH},
Title = {In-vivo studies on the cis-acting replication initiator
protein of IncFII plasmid NR1.},
Journal = {Journal of molecular biology},
Volume = {202},
Number = {3},
Pages = {495-509},
Year = {1988},
Month = {August},
ISSN = {0022-2836},
url = {http://dx.doi.org/10.1016/0022-2836(88)90281-1},
Abstract = {Using segment-directed mutagenesis, a temperature-sensitive
mutant of the gene that encodes the cis-acting RepA1
initiation protein of the IncFII plasmid NR1 was isolated.
The mutant protein was unable to promote initiation of
plasmid replication in vivo at 42 degrees C. Both the
wild-type and the mutant repA1 genes were cloned separately
into the high-expression vector plasmid pAS1. In these
pAS1-repA1 derivatives, the transcription of the repA1 gene
was under the control of the lambda PL promoter, which was
regulated by the temperature-sensitive lambda cI857
repressor protein. The translation initiation of the repA1
mRNA from these derivatives was mediated by the lambda cII
Shine-Dalgarno sequence and initiation codon. The yield of
33,000 Mr RepA1 protein detected on SDS/polyacrylamide gels
from Escherichia coli cells containing the pAS1-repA1
derivatives was dependent upon whether the newly synthesized
RepA1 was capable of interacting in cis with the downstream
NR1 replication origin on the cloned DNA fragment. Mutations
in the repA1 gene or deletions of the cis origin region
dramatically increased the detectable yield of RepA1
protein. Deletion of the NR1 origin region from the pAS1
derivative containing the wild-type repA1 gene enabled the
cis-acting RepA1 protein to complement partially the
temperature-sensitive repA1 mutant in trans, to increase the
copy number in trans of plasmids that contained the NR1
replicon, and to help NR1 derivatives overcome plasmid
incompatibility. The trans effects of RepA1 provided by the
pAS1-repA1 derivatives that retained the origin in cis were
much less significant. RepA1 provided in trans also
stimulated the replication of plasmids carrying cloned
copies of the NR1 replication origin region regardless of
whether the origin was transcribed from an upstream
promoter.},
Doi = {10.1016/0022-2836(88)90281-1},
Key = {fds228337}
}
@article{fds20970,
Author = {Womble, D. D. and X. Dong and R. H. Rownd},
Title = {Changes in RNA secondary structure may mediate the
regulation of IncFII plasmid gene expression and DNA
replication.},
Journal = {In New perspectives on the molecular biology of RNA. M.
Inouye, and B. S. Dudock eds.},
Pages = {225-247},
Year = {1987},
Key = {fds20970}
}
@article{fds228286,
Author = {Dong, X and Womble, DD and Rownd, RH},
Title = {Transcriptional pausing in a region important for plasmid
NR1 replication control.},
Journal = {J. Bacteriol.},
Volume = {169},
Number = {12},
Pages = {353-363},
Year = {1987},
url = {http://dx.doi.org/10.1128/jb.169.12.5353-5363.1987},
Abstract = {The results of in vitro single-round transcription
experiments indicated that RNA polymerase pauses during
transcription of the leader region that precedes the repA1
gene of IncFII plasmid NR1. Transcription initiated at
either of the two transcription promoter sites of the repA1
gene, which encodes the essential replication initiation
protein of NR1, was observed to pause in this region.
Pausing was specifically enhanced by addition of NusA
protein, an Escherichia coli transcription accessory factor.
Northern blot RNA-DNA hybridization analysis of repA1 mRNA
synthesized in vivo revealed RNA species that had lengths
equivalent to those of the in vitro-paused intermediates.
The steady-state rate of in vivo repA1 mRNA transcription
downstream from the pause sites (measured by quantitative
hybridization of pulse-labeled RNA to DNA probes
complementary to different segments of repA1 mRNA) was not
appreciably affected, which suggests that the pause sites do
not promote premature termination of transcription. The
pause sites were located between the target sequence within
the leader region of the mRNA that interacts with a 91-base
countertranscript and the beginning of the repA1 coding
sequence. Because the countertranscript is an inhibitor of
translation of repA1 mRNA, transcriptional pausing in this
region may be an important feature of the regulation of
RepA1 synthesis, which is the mechanism by which plasmid NR1
controls its replication.},
Doi = {10.1128/jb.169.12.5353-5363.1987},
Key = {fds228286}
}
@article{fds20969,
Author = {Rownd, R. H. and D. D. Womble and X. Dong},
Title = {IncFII plasmid replication control and stable
maintenance},
Journal = {In Banbury Report 24: Antibiotic resistance genes: ecology,
transfer, and expression. S. B. Levy, and R. P. Novick
eds.},
Pages = {179-194},
Year = {1986},
Key = {fds20969}
}
@article{fds228338,
Author = {Dong, X and Womble, DD and Luckow, VA and Rownd, RH},
Title = {Regulation of transcription of the repA1 gene in the
replication control region of IncFII plasmid NR1 by gene
dosage of the repA2 transcription repressor
protein.},
Journal = {Journal of bacteriology},
Volume = {161},
Number = {2},
Pages = {544-551},
Year = {1985},
Month = {February},
url = {http://dx.doi.org/10.1128/jb.161.2.544-551.1985},
Abstract = {Transcription of the repA1 gene of the IncFII plasmid NR1 is
initiated at two promoters in the replication control
region. Transcription from the upstream promoter is
constitutive at a low level, whereas transcription from the
downstream promoter is regulated. The 5' end of the
constitutively synthesized transcript also encodes the
transcription repressor protein for the regulated downstream
promoter. Therefore, the level of the repressor protein in
the cell is gene dosage dependent. Using both lac gene
fusions and quantitative hybridization methods, we have
determined the in vivo relationship between the rate of
transcription from the regulated promoter and the repressor
protein concentration as a function of gene dosage. At the
wild-type copy number of NR1, transcription from the
regulated promoter is 96% repressed, but substantial
derepression occurs when the copy number falls below the
normal value. At or above the normal plasmid copy number,
the basal level of repA1 mRNA is provided by transcription
from the constitutive upstream promoter.},
Doi = {10.1128/jb.161.2.544-551.1985},
Key = {fds228338}
}
@article{fds228339,
Author = {Womble, DD and Dong, X and Luckow, VA and Wu, RP and Rownd,
RH},
Title = {Analysis of the individual regulatory components of the
IncFII plasmid replication control system.},
Journal = {Journal of bacteriology},
Volume = {161},
Number = {2},
Pages = {534-543},
Year = {1985},
Month = {February},
ISSN = {0021-9193},
url = {http://dx.doi.org/10.1128/jb.161.2.534-543.1985},
Abstract = {Replication of the IncFII plasmid NR1 is controlled by
regulating the amount of synthesis of the repA1 initiator
protein at both the transcriptional and translational
levels. We have examined mutations which have altered each
of these levels of regulation, resulting in different
plasmid copy numbers. The genes which encode each of the
individual wild-type or mutant regulatory components from
the replication control region of NR1 have been cloned
independently into pBR322 vectors, and their effects in
trans, either individually or in various combinations, on
plasmid incompatibility, stability, copy number, and repA1
gene expression have been defined.},
Doi = {10.1128/jb.161.2.534-543.1985},
Key = {fds228339}
}
@article{fds228287,
Author = {Rownd, RH and Womble, DD and Dong, XN and Luckow, VA and Wu,
RP},
Title = {Incompatibility and IncFII plasmid replication
control.},
Journal = {Basic life sciences},
Volume = {30},
Pages = {335-354},
Year = {1985},
Month = {January},
url = {http://dx.doi.org/10.1007/978-1-4613-2447-8_26},
Abstract = {The DNA coding for replication control and incompatibility
of the plasmid NR1 serves as a template in vivo and in vitro
for RNA transcription in both directions. In the rightward
direction, RNA synthesis begins from 2 different promoters,
one of which is regulated and the other constitutive. In
vivo, each of these transcripts is more than 1,000
nucleotides long, terminating near the estimated site for
the origin of replication. These transcripts serve as
messenger RNA for several proteins. One protein (repA1) is
required for replication and another (repA2) serves as the
repressor for the regulated rightward promoter. RNA
synthesis in the leftward direction is constitutive and
produces a single transcript of 91 nucleotides which is
complementary in sequence to the rightward transcripts. This
small transcript is the incompatibility product which
regulates the replication of the plasmid. When the
intracellular concentration of the small transcript is
experimentally varied, the rate of translation of the
rightward transcripts and the rate of initiation of
replication (plasmid copy number) vary inversely to its
concentration. The mode of action of this inhibitor RNA is
likely to be formation of an RNA-RNA duplex with the
rightward transcripts, thereby inhibiting the translation
which would produce the required replication protein. The
probability that a rightward transcript will escape
interaction with the small RNA molecules and thus allow
replication to initiate can be predicted from the laws of
mass action based on base-stacking free energies for the
likely sequences of initial contact. The estimated
intracellular RNA concentrations, based on quantitative
hybridization experiments, are agreement with those
predicted from the calculated equilibrium constants for
duplex formation.},
Doi = {10.1007/978-1-4613-2447-8_26},
Key = {fds228287}
}
@article{fds228347,
Author = {Womble, DD and Dong, X and Wu, RP and Luckow, VA and Martinez, AF and Rownd, RH},
Title = {IncFII plasmid incompatibility product and its target are
both RNA transcripts.},
Journal = {Journal of bacteriology},
Volume = {160},
Number = {1},
Pages = {28-35},
Year = {1984},
Month = {October},
ISSN = {0021-9193},
url = {http://dx.doi.org/10.1128/jb.160.1.28-35.1984},
Abstract = {The region of DNA coding for incompatibility (inc) and copy
number control (cop) of the IncFII plasmid NR1 is
transcribed in both the rightward and leftward directions.
The rightward transcripts serve as mRNA for the repA1
protein, which is required for replication. A small, 91-base
leftward transcript is synthesized from the opposite DNA
strand and is complementary to a portion of the rightward
mRNA near its 5' end. A 262-base-pair Sau3A restriction
fragment that encodes the small leftward transcript, but
does not include the rightward transcription promoters, was
cloned into the vector pBR322 or pUC8. The same fragment was
cloned from an Inc- mutant of NR1 that does not make the
small leftward transcript. Transcription through the cloned
fragments in these derivatives was under control of the
tetracycline resistance gene in pBR322 or the lac
promoter-operator in pUC8. In one orientation of the
inserted DNA, a hybrid transcript containing rightward NR1
RNA sequences was synthesized. In the other orientation, a
hybrid transcript containing leftward NR1 RNA sequences was
synthesized. These plasmids were used to vary the
intracellular levels of the rightward or leftward NR1 RNA
transcripts and to test their effects in trans on various
coresident derivatives of NR1. An excess of rightward NR1
RNA in trans stimulated expression of the essential repA1
gene and caused an increase in the copy number of a
coresident NR1 plasmid. An excess of leftward NR1 RNA in
trans inhibited the expression of the repA1 gene and lowered
the coresident NR1 copy number, thereby causing
incompatibility. A pBR322 derivative with no transcription
through the cloned NR1 DNA had no effect in trans. These
results suggest that the small leftward transcript is the
incompatibility inhibitor of NR1 and that its target is the
complementary portion of the rightward mRNA.},
Doi = {10.1128/jb.160.1.28-35.1984},
Key = {fds228347}
}