Publications of Xinnian Dong :chronological combined listing:
%% Papers Published
@article{fds158995,
Author = {SH Spoel and Z Mou and Y Tada and NW Spivey and P Genschik and X
Dong},
Title = {Proteasome-mediated turnover of the transcription
coactivator NPR1 plays dual roles in regulating plant
immunity.},
Journal = {Cell},
Volume = {137},
Pages = {860-72},
Year = {2009},
Month = {May},
ISSN = {1097-4172},
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.},
Key = {fds158995}
}
@article{fds152257,
Author = {Spoel, S. H. and Dong, X},
Title = {Making sense of hormone crosstalk during
plant},
Journal = {Cell Host & Microbe},
Volume = {3},
Pages = {348-351},
Year = {2008},
Key = {fds152257}
}
@article{fds147802,
Author = {Tada, Y. and Spoel, S. H. and Pajerowska-Mukhtar, 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},
Year = {2008},
url = {http://www.sciencemag.org/cgi/rapidpdf/1156970?ijkey=/8he5p3s6CA6g&keytype=ref&siteid=sci},
Abstract = {http://www.sciencemag.org/cgi/content/abstract/1156970?ijkey=/8he5p3s6CA6g&keytype=ref&siteid=sci},
Key = {fds147802}
}
@article{fds139263,
Author = {SH Spoel and JS Johnson and X Dong},
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, United States},
Volume = {104},
Number = {47},
Pages = {18842-7},
Year = {2007},
Month = {November},
ISSN = {1091-6490},
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.},
Key = {fds139263}
}
@article{fds139261,
Author = {X Zhang and Y Dai and Y Xiong and C Defraia and J Li and X Dong and Z
Mou},
Title = {Overexpression of Arabidopsis MAP kinase kinase 7 leads to
activation of plant basal and systemic acquired
resistance.},
Journal = {Plant J},
Year = {2007},
Month = {October},
ISSN = {0960-7412},
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.},
Key = {fds139261}
}
@article{fds139262,
Author = {D Wang and K Pajerowska-Mukhtar and AH Culler and X
Dong},
Title = {Salicylic acid inhibits pathogen growth in plants through
repression of the auxin signaling pathway.},
Journal = {Current biology : CB, England},
Volume = {17},
Number = {20},
Pages = {1784-90},
Year = {2007},
Month = {October},
ISSN = {0960-9822},
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.},
Key = {fds139262}
}
@article{fds139264,
Author = {C Xue and Y Tada and X Dong and J Heitman},
Title = {The human fungal pathogen Cryptococcus can complete its
sexual cycle during a pathogenic association with
plants.},
Journal = {Cell host & microbe, United States},
Volume = {1},
Number = {4},
Pages = {263-73},
Year = {2007},
Month = {June},
ISSN = {1934-6069},
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.},
Key = {fds139264}
}
@article{fds139260,
Author = {M Kesarwani and J Yoo and X Dong},
Title = {Genetic interactions of TGA transcription factors in the
regulation of pathogenesis-related genes and disease
resistance in Arabidopsis.},
Journal = {Plant physiology, United States},
Volume = {144},
Number = {1},
Pages = {336-46},
Year = {2007},
Month = {May},
ISSN = {0032-0889},
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.},
Key = {fds139260}
}
@article{fds139259,
Author = {WE Durrant and S Wang and X Dong},
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, United States},
Volume = {104},
Number = {10},
Pages = {4223-7},
Year = {2007},
Month = {March},
ISSN = {0027-8424},
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.},
Key = {fds139259}
}
@article{fds52605,
Author = {RA Mosher and WE Durrant and D Wang and J Song and X
Dong},
Title = {A comprehensive structure-function analysis of Arabidopsis
SNI1 defines essential regions and transcriptional repressor
activity.},
Journal = {Plant Cell, United States},
Volume = {18},
Number = {7},
Pages = {1750-65},
Year = {2006},
Month = {July},
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.},
Key = {fds52605}
}
@article{fds52607,
Author = {Heidel, A.J. and Dong, X.},
Title = {Fitness benefits of systemic acquired resistance during
Hyaloperonospora parasitica infection in Arabidopsis
thaliana},
Journal = {Genetics},
Volume = {173},
Pages = {1621-1628},
Year = {2006},
Key = {fds52607}
}
@article{fds52608,
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},
Pages = {1042-1050},
Year = {2006},
Key = {fds52608}
}
@article{fds37918,
Author = {Dong, W. and Weaver, N.D. and Kesarwani, M. and Dong, X.},
Title = {Induction of Protein Secretory Pathway Is Required for
Systemic Acquired Resistance},
Journal = {Science},
Volume = {308},
Pages = {1036-1040},
Year = {2005},
Key = {fds37918}
}
@article{fds20954,
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 = {www.stke.org/cgi/content/full/sigtrans;2004/221/pe6},
Key = {fds20954}
}
@article{fds29447,
Author = {W. E. Durrant and X. Dong},
Title = {Systemic acquired resistance},
Journal = {Annual Review of Phytopathology},
Volume = {42},
Pages = {185-209},
Year = {2004},
Key = {fds29447}
}
@article{fds29449,
Author = {X. Dong},
Title = {NPR1. all things considered},
Journal = {Current Opinion in Plant Biology},
Volume = {7},
Pages = {547-552},
Year = {2004},
Key = {fds29449}
}
@article{fds20953,
Author = {Dong, X.},
Title = {Pathogen-induced systemic DNA rearrangement in
plants},
Journal = {Trends in Plant Science},
Volume = {9},
Pages = {60-61},
Year = {2004},
Key = {fds20953}
}
@article{fds29987,
Author = {A. Heidel and J. D. Clarke and J. Antonovics and X.
Dong},
Title = {Fitness costs of mutants affecting the systemicacquired
resistance pathway in Arabidopsis thaliana},
Journal = {Genetics},
Volume = {168},
Pages = {2197-2206},
Year = {2004},
Key = {fds29987}
}
@article{fds17154,
Author = {Spoel, S. H. and Koornneef, A. and Claessens, S. M. C. and Korzelius
J. P. and Van Pelt and J. A. and Mueller, M. J. and Buchala, A. J. and Métraux J.-P. and Brown, R. and Kazan, K. and Van Loon and L.C., Dong and X. and Pieterse C. M. J.},
Title = {NPR1 modulates cross talk between salicylate- and
jasmonate-dependent plant defense pathways through a novel
function in the cytosol.},
Journal = {Plant Cell},
Volume = {15},
Pages = {760},
Year = {2003},
Key = {fds17154}
}
@article{fds17155,
Author = {Mou, Z. Fan and W. and Dong, X.},
Title = {Inducers of plant systemic acquired resistance regulate NPR1
function through redox changes.},
Journal = {Cell},
Volume = {113},
Pages = {935},
Year = {2003},
Key = {fds17155}
}
@article{fds17156,
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},
Pages = {2636},
Year = {2003},
Key = {fds17156}
}
@article{fds17153,
Author = {Fan, W. and Dong, X},
Title = {In Vivo Interaction between NPR1 and transcription},
Journal = {Plant Cell},
Volume = {14},
Pages = {1377},
Year = {2002},
Key = {fds17153}
}
@article{fds17151,
Author = {Li X. and Clarke J. D. 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},
Volume = {14},
Pages = {1131},
Year = {2001},
Key = {fds17151}
}
@article{fds17152,
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},
Year = {2001},
Key = {fds17152}
}
@article{fds20958,
Author = {Dong, X.},
Title = {Genetic dissection of systemic acquired resistance},
Journal = {Current Opinion in Plant Biology},
Volume = {4},
Pages = {309-314},
Year = {2001},
Key = {fds20958}
}
@article{fds20959,
Author = {Jirage, D. and Zhou, N. and Cooper, B. and Clarke, J.D. and Dong, X. and Glazebrook, J.},
Title = {Constitutive salicylic acid-dependent signaling in cpr1 and
cpr6 mutants requires PAD4.},
Journal = {Plant J.},
Volume = {26},
Pages = {395-408},
Year = {2001},
Key = {fds20959}
}
@article{fds20960,
Author = {Chern, M.-S. and Fitzgerald, H.A and . Yadav, R.C. and Canlas, P.E. and Dong, X. and Ronald, P.C.},
Title = {Evidence for a disease-resistance pathway in rice similar to
the NPR1-mediated signaling pathway in Arabidopsis},
Journal = {Plant J.},
Volume = {27},
Pages = {101-113},
Year = {2001},
Key = {fds20960}
}
@article{fds20961,
Author = {Clarke, J.D. and Aarts, N. and Feys, B.J. and Dong, X. and Parker
J.E.},
Title = {Constitutive disease resistance requires ESD1 in the
Arabidopsis mutants cpr1 and is partially EDS1-dependent in
cpr5},
Journal = {Plant J.},
Volume = {26},
Pages = {409-420},
Year = {2001},
Key = {fds20961}
}
@article{fds20962,
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},
Pages = {235-242},
Year = {2001},
Key = {fds20962}
}
@article{fds20963,
Author = {Kinkema, M. and Fan, W. and Dong, X.},
Title = {Nuclear localization of NPR1 is required for activation of
PR gene expression},
Journal = {Plant Cell},
Volume = {12},
Pages = {2339-2350},
Year = {2000},
Key = {fds20963}
}
@article{fds20964,
Author = {Clarke, J.D. and Volko, S.M. and Ledford, H. and Ausubel, F.M. and Dong, X.},
Title = {Roles of salicylic acid, jasmonic acid, and ethylene in
cpr-induces resistance in Arabidopsis},
Journal = {Plant Cell},
Volume = {12},
Pages = {2175-2190},
Year = {2000},
Key = {fds20964}
}
@article{fds17149,
Author = {Zhang, Y. and Fan, W. and Kinkema, M. and Li, Xin 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 = {Proc. Natl. Acad. Sci. USA},
Volume = {96},
Pages = {6523},
Year = {1999},
Key = {fds17149}
}
@article{fds17150,
Author = {Li, X. and Zhang, Y. and Clarke, J.D. 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},
Pages = {329},
Year = {1999},
Key = {fds17150}
}
@article{fds20986,
Author = {Cao, H. and X. Li and X. Dong},
Title = {Generation of broad-spectrum disease resistance by
overexpression of an essential regulatory gene in systemic
acquired resistance.},
Journal = {Proc. Natl. Acad. Sci. USA},
Volume = {95},
Pages = {6531-6536},
Year = {1998},
Key = {fds20986}
}
@article{fds20987,
Author = {Clarke, J. D. and Liu, Y. and Klessig, D. F. and X.
Dong},
Title = {Uncoupling PR-gene expression from NPR1 and bacterial
resistance: Characterization of the dominant Arabidopsis
cpr6 mutant.},
Journal = {Plant Cell},
Volume = {10},
Pages = {557-567},
Year = {1998},
Key = {fds20987}
}
@article{fds20988,
Author = {Dong, X.},
Title = {SA, JA, ethylene, and disease resistance in
plants.},
Journal = {Current Opinion in Plant Biology},
Volume = {1},
Pages = {316-323},
Year = {1998},
Key = {fds20988}
}
@article{fds20984,
Author = {Cao, H. and J. Glazebrook and J. D. Clarke and S. Volko and X.
Dong.},
Title = {The Arabidopsis NPR1 gene that controls systemic acquired
resistance encodes a novel protein containing ankyrin
repeats.},
Journal = {Cell},
Volume = {88},
Pages = {57-63},
Year = {1997},
Key = {fds20984}
}
@article{fds20985,
Author = {Bowling, S. A. and J. D. Clarke and Y. Liu and D. F. Klessig and X.
Dong.},
Title = {The cpr5 mutant of Arabidopsis expresses both NPR1-dependent
and NPR1-independent resistance.},
Journal = {Plant Cell},
Volume = {9},
Pages = {1573-1584},
Year = {1997},
Key = {fds20985}
}
@article{fds20983,
Author = {Dong, X.},
Title = {Finding the missing pieces in the puzzle of plant disease
resistance.},
Journal = {Proc. Natl. Acad. Sci. USA},
Volume = {92},
Pages = {7137-7139},
Year = {1995},
Key = {fds20983}
}
@article{fds20981,
Author = {Cao, H. and S. A. Bowling and A. S. Gordon and X.
Dong},
Title = {Characterization of an Arabidopsis mutant that is
nonresponsive to inducers of systemic acquired
resistance.},
Journal = {Plant Cell},
Volume = {6},
Pages = {1583-1592},
Year = {1994},
Key = {fds20981}
}
@article{fds20982,
Author = {Bowling, S. A. and A. Guo and H. Cao and A. S. Gordon and D. F. Klessig and X. Dong.},
Title = {A mutation in Arabidopsis that leads to constitutive
expression of systemic acquired resistance.},
Journal = {Plant Cell},
Volume = {6},
Pages = {1845-1857},
Year = {1994},
Key = {fds20982}
}
@article{fds20980,
Author = {Melan, M. A. and X. Dong and M. E. Endara and K. R. Davis and F. M.
Ausubel and T. K. Peterman.},
Title = {An Arabidopsis thaliana lipoxygenase gene is induced by
pathogens, abscisic acid and methyl jasmonate.},
Journal = {Plant Physiol.},
Volume = {101},
Pages = {441-450},
Year = {1993},
Key = {fds20980}
}
@article{fds20977,
Author = {Dong, X. and M. Mindrinos and K.R. Davis and F.M.
Ausubel.},
Title = {Induction of Arabidopsis thaliana defense genes by virulent
and avirulent Pseudomonas syringae strains and by a cloned
avirulent gene.},
Journal = {Plant Cell},
Volume = {3},
Pages = {61-72},
Year = {1991},
Key = {fds20977}
}
@article{fds20979,
Author = {Keith, B. and X. Dong and F. Ausubel and G. Fink},
Title = {Differential induction of 3-deoxy-D-arabino-heptulosonate
7-phosphate synthase genes in Arabidopsis thaliana by
wounding and pathogenic attack},
Journal = {Proc. Natl. Acad. Sci. USA.},
Volume = {88},
Pages = {8821-8825},
Year = {1991},
Key = {fds20979}
}
@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{fds20973,
Author = {Dong, X. and K. P. Rouillard and D. D. Womble and R. H.
Rownd},
Title = {DNA bending near the replication origin of IncFII plasmid
NR1.},
Journal = {J. Bacteriol.},
Volume = {171},
Pages = {703-707},
Year = {1989},
Key = {fds20973}
}
@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{fds20972,
Author = {Dong, X. and D. D. Womble and R. H. Rownd},
Title = {). In vivo studies on the cis-acting replication initiator
protein of IncFII plasmid NR1.},
Journal = {J. Mol. Biol.},
Volume = {202},
Pages = {495-509},
Year = {1988},
Key = {fds20972}
}
@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{fds20971,
Author = {Dong, X. and D. D. Womble and R. H. Rownd},
Title = {Transcriptional pausing in a region important for plasmid
NR1 replication control.},
Journal = {J. Bacteriol.},
Volume = {169},
Pages = {353-363},
Year = {1987},
Key = {fds20971}
}
@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{fds20965,
Author = {Rownd, R. H. and D. D. Womble and X. Dong and V. A. Luckow and R.-P.
Wu.},
Title = {Incompatibility and IncFII plasmid replication
control},
Journal = {In Plasmid in bacteria. D. R. Helinski, S. N. Cohen, D. B.
Clewell, D. A. Jackson, and A. Hollaender
eds.},
Pages = {335-354},
Year = {1985},
Key = {fds20965}
}
@article{fds20966,
Author = {Womble, D. D. and X. Dong and V. A. Luckow and R. P. Wu and R. H.
Rownd.},
Title = {Analysis of the individual regulatory components of the
IncFII plasmid replication control system},
Journal = {J. Bacteriol.},
Volume = {161},
Pages = {534-543},
Year = {1985},
Key = {fds20966}
}
@article{fds20968,
Author = {Dong, X. and D. D. Womble and V. A. Luckow and R. H.
Rownd},
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 = {J. Bacteriol.},
Volume = {161},
Pages = {544-551},
Year = {1985},
Key = {fds20968}
}
@article{fds20956,
Author = {Womble, D. D. and X. Dong and R.-P. Wu and V. A. Luckow and A. F.
Martinez and R. H. Rownd},
Title = {IncFII plasmid incompatibility product and its target are
both RNA transcripts},
Journal = {J. Bacteriol},
Volume = {160},
Pages = {28},
Year = {1984},
Key = {fds20956}
}
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