Publications of David R. Sherwood :chronological combined listing:
%% Papers Published
@article{fds161088,
Author = {EJ Hagedorn and H Yashiro and JW Ziel and S Ihara and Z Wang and DR
Sherwood},
Title = {Integrin acts upstream of netrin signaling to regulate
formation of the anchor cell's invasive membrane in C.
elegans.},
Journal = {Developmental cell, United States},
Volume = {17},
Number = {2},
Pages = {187-98},
Year = {2009},
Month = {August},
ISSN = {1878-1551},
Abstract = {Integrin expression and activity have been strongly
correlated with developmental and pathological processes
involving cell invasion through basement membranes. The role
of integrins in mediating these invasions, however, remains
unclear. Utilizing the genetically and visually accessible
model of anchor cell (AC) invasion in C. elegans, we have
recently shown that netrin signaling orients a specialized
invasive cell membrane domain toward the basement membrane.
Here, we demonstrate that the integrin heterodimer
INA-1/PAT-3 plays a crucial role in AC invasion, in part by
targeting the netrin receptor UNC-40 (DCC) to the AC's
plasma membrane. Analyses of the invasive membrane
components phosphatidylinositol 4,5-bisphosphate, the Rac
GTPase MIG-2, and F-actin further indicate that INA-1/PAT-3
plays a broad role in promoting the plasma membrane
association of these molecules. Taken together, these
studies reveal a role for integrin in regulating the plasma
membrane targeting and netrin-dependent orientation of a
specialized invasive membrane domain.},
Key = {fds161088}
}
@article{fds159350,
Author = {JW Ziel and DQ Matus and DR Sherwood},
Title = {An expression screen for RhoGEF genes involved in C. elegans
gonadogenesis.},
Journal = {Gene expression patterns : GEP},
Year = {2009},
Month = {June},
ISSN = {1567-133X},
Abstract = {The gonad in C. elegans is an important model system for
understanding complex morphogenetic processes including
cellular movement, cell fusion, cell invasion and cell
polarity during development. One class of signaling proteins
known to be critical for the cellular events underlying
morphogenesis is the Rho family GTPases, particularly RhoA,
Rac and Cdc42. In C. elegans orthologues of these genes have
been shown to be important for gonad development. In our
current study we have extended those findings by examining
the patterns of 5'cis-regulatory element (5'CRE) activity
associated with nineteen putative guanine nucleotide
exchange factors (GEFs) encoded by the C. elegans genome
predicted to activate Rho family GTPases. Here we identify
thirteen RhoGEF genes that are expressed during
gonadogenesis and characterize the cells in which their
5'CREs are active. These data provide the basis for
designing experiments to examine Rho GTPase activation
during morphogenetic processes central to normal gonad
development.},
Key = {fds159350}
}
@article{fds159352,
Author = {D Sherwood},
Title = {David Sherwood: invasive procedures. Interview by Ben
Short.},
Journal = {The Journal of cell biology, United States},
Volume = {185},
Number = {4},
Pages = {568-9},
Year = {2009},
Month = {May},
ISSN = {1540-8140},
Keywords = {Animals • Basement Membrane • Biomedical Research
• Caenorhabditis elegans • Cell Movement* •
History, 20th Century • History, 21st Century •
Humans • Models, Animal • Neoplasm Invasiveness*
• United States • metabolism},
Key = {fds159352}
}
@article{fds159351,
Author = {JW Ziel and EJ Hagedorn and A Audhya and DR Sherwood},
Title = {UNC-6 (netrin) orients the invasive membrane of the anchor
cell in C. elegans.},
Journal = {Nature cell biology, England},
Volume = {11},
Number = {2},
Pages = {183-9},
Year = {2009},
Month = {February},
ISSN = {1476-4679},
Keywords = {Actins • Animals • Animals, Genetically Modified
• Basement Membrane • Caenorhabditis elegans
• Caenorhabditis elegans Proteins • Cell Adhesion
Molecules • Cell Membrane • Cell Polarity •
Female • Genitalia, Female • Models, Animal •
Neoplasm Invasiveness • Nerve Tissue Proteins •
Phosphatidylinositol 4,5-Diphosphate • Signal
Transduction • Stem Cells • cytology •
embryology • genetics • metabolism •
metabolism* • physiology • physiology* •
physiopathology • ultrastructure},
Abstract = {Despite their profound importance in the development of
cancer, the extracellular cues that target cell invasion
through basement membrane barriers remain poorly understood.
A central obstacle has been the difficulty of studying the
interactions between invading cells and basement membranes
in vivo. Using the genetically and visually tractable model
of Caenorhabditis elegans anchor cell (AC) invasion, we show
that UNC-6 (netrin) signalling, a pathway not previously
implicated in controlling cell invasion in vivo, is a key
regulator of this process. Site of action studies reveal
that before invasion, localized UNC-6 secretion directs its
receptor, UNC-40, to the plasma membrane of the AC, in
contact with the basement membrane. There, UNC-40 polarizes
a specialized invasive membrane domain through the
enrichment of actin regulators, F-actin and
phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)).
Cell ablation experiments indicate that UNC-6 promotes the
formation of invasive protrusions from the AC that break
down the basement membrane in response to a subsequent
vulval cue. Together, these results characterize an invasive
membrane domain in vivo, and reveal a role for UNC-6
(netrin) in polarizing this domain towards its basement
membrane target.},
Key = {fds159351}
}
@article{fds48749,
Author = {DR Sherwood},
Title = {Cell invasion through basement membranes: an anchor of
understanding.},
Journal = {Trends Cell Biol, England},
Volume = {16},
Number = {5},
Pages = {250-6},
Year = {2006},
Month = {May},
Abstract = {To metastasize, cancer cells must acquire the ability to
breach several basement membrane barriers. Cell invasions
through basement membranes also occur during normal
development and immune system function, enabling organ
formation and cell dispersal. The mechanisms that cells use
to cross basement membranes in vivo remain elusive. In
cancer and development, these invasions occur in complex and
inaccessible environments, which are difficult to study in
vivo. Anchor-cell invasion in Caenorhabditis elegans is a
simple, visually and experimentally accessible model of
basement membrane invasion that is beginning to reveal a
network of cellular and molecular control mechanisms that
regulate the fundamental cellular process of invasion
through basement membranes.},
Key = {fds48749}
}
@article{fds38896,
Author = {DR Sherwood and JA Butler and JM Kramer and PW Sternberg},
Title = {FOS-1 promotes basement-membrane removal during anchor-cell
invasion in C. elegans.},
Journal = {Cell, United States},
Volume = {121},
Number = {6},
Pages = {951-62},
Year = {2005},
Month = {June},
Abstract = {Cell invasion through basement membranes is crucial during
morphogenesis and cancer metastasis. Here, we genetically
dissect this process during anchor-cell invasion into the
vulval epithelium in C. elegans. We have identified the fos
transcription factor ortholog fos-1 as a critical regulator
of basement-membrane removal. In fos-1 mutants, the gonadal
anchor cell extends cellular processes normally toward
vulval cells, but these processes fail to remove the
basement membranes separating the gonad from the vulval
epithelium. fos-1 is expressed in the anchor cell and
controls invasion cell autonomously. We have identified
ZMP-1, a membrane-type matrix metalloproteinase, CDH-3, a
Fat-like protocadherin, and hemicentin, a fibulin family
extracellular matrix protein, as transcriptional targets of
FOS-1 that promote invasion. These results reveal a key
genetic network that controls basement-membrane removal
during cell invasion.},
Key = {fds38896}
}
@article{fds38898,
Author = {DR Sherwood and PW Sternberg},
Title = {Anchor cell invasion into the vulval epithelium in C.
elegans.},
Journal = {Dev Cell, United States},
Volume = {5},
Number = {1},
Pages = {21-31},
Year = {2003},
Month = {July},
Abstract = {An understanding of cell-invasive behavior has been limited
by the lack of in vivo models where this activity can be
clearly visualized and manipulated. We show that a single
cell in the Caenorhabditis elegans gonad, the anchor cell
(AC), initiates uterine-vulval contact through a cell
invasion event. Using genetic analysis, laser ablations, and
cell-specific markers, we demonstrate that AC invasion is
predominantly stimulated by the 1 degrees vulval lineage
cells, which generate a diffusible signal that promotes AC
invasive behavior toward these cells and further targets
invasive processes between the two central 1 degrees vulval
lineage cells. We also show that AC invasion is regulated by
the AC response to this cue, as well as a vulval-independent
mechanism that weakly drives invasion. These studies dissect
the regulatory mechanisms that underlie a simple
cell-invasive behavior in vivo, and introduce AC invasion as
a model for understanding key checkpoints controlling cell
invasion.},
Key = {fds38898}
}
@article{fds38897,
Author = {T Inoue and DR Sherwood and G Aspöck and JA Butler and BP Gupta and M
Kirouac, M Wang and PY Lee and JM Kramer and I Hope and TR Bürglin and PW Sternberg},
Title = {Gene expression markers for Caenorhabditis elegans vulval
cells.},
Journal = {Mech Dev, Ireland},
Volume = {119 Suppl 1},
Pages = {S203-9},
Year = {2002},
Month = {December},
Abstract = {The analysis of cell fate patterning during the vulval
development of Caenorhabditis elegans has relied mostly on
the direct observation of cell divisions and cell movements
(cell lineage analysis). However, reconstruction of the
developing vulva from EM serial sections has suggested seven
different cell types (vulA, vulB1, vulB2, vulC, vulD, vulE,
and vulF), many of which cannot be distinguished based on
such observations. Here we report the vulval expression of
seven genes, egl-17, cdh-3, ceh-2, zmp-1, B0034.1, T04B2.6
and F47B8.6 based on gfp, cfp and yfp (green fluorescent
protein and color variants) reporter fusions. Each gene
expresses in a specific subset of vulval cells, and is
therefore useful as a marker for vulval cell fates.
Together, expressions of markers distinguish six cell types,
and reveal a strict temporal control of gene expression in
the developing vulva.},
Key = {fds38897}
}
@article{fds38899,
Author = {T Inoue and DR Sherwood and G Aspöck and JA Butler and BP Gupta and M
Kirouac, M Wang and PY Lee and JM Kramer and I Hope and TR Bürglin and PW Sternberg},
Title = {Gene expression markers for Caenorhabditis elegans vulval
cells.},
Journal = {Gene Expr Patterns, Unknown},
Volume = {2},
Number = {3-4},
Pages = {235-41},
Year = {2002},
Month = {December},
Abstract = {The analysis of cell fate patterning during the vulval
development of Caenorhabditis elegans has relied mostly on
the direct observation of cell divisions and cell movements
(cell lineage analysis). However, reconstruction of the
developing vulva from EM serial sections has suggested seven
different cell types (vulA, vulB1, vulB2, vulC, vulD, vulE,
and vulF), many of which cannot be distinguished based on
such observations. Here we report the vulval expression of
seven genes, egl-17, cdh-3, ceh-2, zmp-1, B0034.1, T04B2.6
and F47B8.6 based on gfp, cfp and yfp (green fluorescent
protein and color variants) reporter fusions. Each gene
expresses in a specific subset of vulval cells, and is
therefore useful as a marker for vulval cell fates.
Together, expressions of markers distinguish six cell types,
and reveal a strict temporal control of gene expression in
the developing vulva.},
Key = {fds38899}
}
@article{fds38900,
Author = {RE Palmer and T Inoue and DR Sherwood and LI Jiang and PW
Sternberg},
Title = {Caenorhabditis elegans cog-1 locus encodes GTX/Nkx6.1
homeodomain proteins and regulates multiple aspects of
reproductive system development.},
Journal = {Dev Biol, United States},
Volume = {252},
Number = {2},
Pages = {202-13},
Year = {2002},
Month = {December},
Abstract = {The development of the reproductive system in Caenorhabditis
elegans is a well-established model system for patterning
and organogenesis. We report the characterization of the
cog-1 gene, mutations in which cause novel phenotypes in
late patterning in vulval lineages, establishment of the
vulva-uterine connection, development and function of the
spermathecal-uterine junction, and the development of vas
deferens-proctodeal connection in the male. We positionally
cloned cog-1 and found that it encodes a homeobox protein
most similar to the mammalian GTX and Nkx6.1 proteins.
Analysis of cog-1 transcripts revealed that cog-1 is likely
a complex locus with two promoters. Two mutant alleles of
cog-1 differentially affect alternative transcripts and
cause different phenotypes, suggesting that the two forms of
cog-1 have distinct functions in C. elegans.},
Key = {fds38900}
}
@article{fds38901,
Author = {DR Sherwood and DR McClay},
Title = {LvNotch signaling plays a dual role in regulating the
position of the ectoderm-endoderm boundary in the sea urchin
embryo.},
Journal = {Development, England},
Volume = {128},
Number = {12},
Pages = {2221-32},
Year = {2001},
Month = {June},
Abstract = {The molecular mechanisms guiding the positioning of the
ectoderm-endoderm boundary along the animal-vegetal axis of
the sea urchin embryo remain largely unknown. We report here
a role for the sea urchin homolog of the Notch receptor,
LvNotch, in mediating the position of this boundary.
Overexpression of an activated form of LvNotch throughout
the embryo shifts the ectoderm-endoderm boundary more
animally along the animal-vegetal axis, whereas expression
of a dominant negative form shifts the border vegetally.
Mosaic experiments that target activated and dominant
negative forms of LvNotch into individual blastomeres of the
early embryo, combined with lineage analyses, further reveal
that LvNotch signaling mediates the position of this
boundary by distinct mechanisms within the animal versus
vegetal portions of the embryo. In the animal region of the
embryo, LvNotch signaling acts cell autonomously to promote
endoderm formation more animally, while in the vegetal
portion, LvNotch signaling also promotes the
ectoderm-endoderm boundary more animally, but through a cell
non-autonomous mechanism. We further demonstrate that
vegetal LvNotch signaling controls the localization of
nuclear beta-catenin at the ectoderm-endoderm boundary.
Based on these results, we propose that LvNotch signaling
promotes the position of the ectoderm-endoderm boundary more
animally via two mechanisms: (1) a cell-autonomous function
within the animal region of the embryo, and (2) a cell
non-autonomous role in the vegetal region that regulates a
signal(s) mediating ectoderm-endoderm position, possibly
through the control of nuclear beta-catenin at the
boundary.},
Key = {fds38901}
}
@article{fds38902,
Author = {DR Sherwood and DR McClay},
Title = {LvNotch signaling mediates secondary mesenchyme
specification in the sea urchin embryo.},
Journal = {Development, ENGLAND},
Volume = {126},
Number = {8},
Pages = {1703-13},
Year = {1999},
Month = {April},
Abstract = {Cell-cell interactions are thought to regulate the
differential specification of secondary mesenchyme cells
(SMCs) and endoderm in the sea urchin embryo. The molecular
bases of these interactions, however, are unknown. We have
previously shown that the sea urchin homologue of the
LIN-12/Notch receptor, LvNotch, displays dynamic patterns of
expression within both the presumptive SMCs and endoderm
during the blastula stage, the time at which these two cell
types are thought to be differentially specified (Sherwood,
D. R. and McClay, D. R. (1997) Development 124, 3363-3374).
The LIN-12/Notch signaling pathway has been shown to mediate
the segregation of numerous cell types in both invertebrate
and vertebrate embryos. To directly examine whether LvNotch
signaling has a role in the differential specification of
SMCs and endoderm, we have overexpressed activated and
dominant negative forms of LvNotch during early sea urchin
development. We show that activation of LvNotch signaling
increases SMC specification, while loss or reduction of
LvNotch signaling eliminates or significantly decreases SMC
specification. Furthermore, results from a mosaic analysis
of LvNotch function as well as endogenous LvNotch expression
strongly suggest that LvNotch signaling acts autonomously
within the presumptive SMCs to mediate SMC specification.
Finally, we demonstrate that the expansion of SMCs seen with
activation of LvNotch signaling comes at the expense of
presumptive endoderm cells, while loss of SMC specification
results in the endoderm expanding into territory where SMCs
usually arise. Taken together, these results offer
compelling evidence that LvNotch signaling directly
specifies the SMC fate, and that this signaling is critical
for the differential specification of SMCs and endoderm in
the sea urchin embryo.},
Key = {fds38902}
}
@article{fds38903,
Author = {DR Sherwood and DR McClay},
Title = {Identification and localization of a sea urchin Notch
homologue: insights into vegetal plate regionalization and
Notch receptor regulation.},
Journal = {Development, ENGLAND},
Volume = {124},
Number = {17},
Pages = {3363-74},
Year = {1997},
Month = {September},
Abstract = {The specifications of cell types and germ-layers that arise
from the vegetal plate of the sea urchin embryo are thought
to be regulated by cell-cell interactions, the molecular
basis of which are unknown. The Notch intercellular
signaling pathway mediates the specification of numerous
cell fates in both invertebrate and vertebrate development.
To gain insights into mechanisms underlying the
diversification of vegetal plate cell types, we have
identified and made antibodies to a sea urchin homolog of
Notch (LvNotch). We show that in the early blastula embryo,
LvNotch is absent from the vegetal pole and concentrated in
basolateral membranes of cells in the animal half of the
embryo. However, in the mesenchyme blastula embryo LvNotch
shifts strikingly in subcellular localization into a ring of
cells which surround the central vegetal plate. This ring of
LvNotch delineates a boundary between the presumptive
secondary mesoderm and presumptive endoderm, and has an
asymmetric bias towards the dorsal side of the vegetal
plate. Experimental perturbations and quantitative analysis
of LvNotch expression demonstrate that the mesenchyme
blastula vegetal plate contains both animal/vegetal and
dorsoventral molecular organization even before this
territory invaginates to form the archenteron. Furthermore,
these experiments suggest roles for the Notch pathway in
secondary mesoderm and endoderm lineage segregation, and in
the establishment of dorsoventral polarity in the endoderm.
Finally, the specific and differential subcellular
expression of LvNotch in apical and basolateral membrane
domains provides compelling evidence that changes in
membrane domain localization of LvNotch are an important
aspect of Notch receptor function.},
Key = {fds38903}
}
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