ライフサイエンスコーパス: vulval

1 rived LIN-3 EGF signal and adopt the uterine vulval 1 (uv1) fate.

2 represented sequences involved in conferring vulval and AC expression.

3 omatic gonad epithelium, and show defects in vulval and excretory cell epithelia and in motoneuron ax

4 uction of hda-1 RNA by RNAi causes defective vulval and gonadal development leading to sterility.

5 ets of genes to regulate G(1)/S progression, vulval and pharyngeal differentiation, and other unknown

6 6 mutations described herein cause delays in vulval and seam cell differentiation, indicating a role

7 nts appear to have no connection between the vulval and the uterine lumens at the appropriate stage b

8 We study Caenorhabditis elegans vulval and uterine development to probe the complex mech

9 is expressed in pharyngeal, anal depressor, vulval and uterine muscles and in spermatheca and intest

10 aled that unc-94a is expressed in body wall, vulval and uterine muscles, whereas unc-94b is expressed

11 Here we analyse uterine-vulval attachment during development across 21 species o

12 imilar risk factors have been highlighted in vulval cancer.

13 ively with the lin-39 Hox gene in regulating vulval cell differentiation.

14 We show that most vulval cell divisions produce sister cells that have asy

15 quired for the proper orientation of certain vulval cell divisions, suggesting a role in spindle posi

16 tion of lin-1 as an inhibitor of the primary vulval cell fate and also reduce DNA binding suggest tha

17 LIN-1 in the P6.p cell to induce the primary vulval cell fate during Caenorhabditis elegans developme

18 ndant classes, A and B, that repress ectopic vulval cell fate induction.

19 nt signaling pathway, to negatively regulate vulval cell fate specification.

20 tem development, P12 fate specification, and vulval cell fate specification.

21 ursor cells occasionally adopt the 3 degrees vulval cell fate, resulting in a deformed vulva, and the

22 By examining GFP markers of dorsal vulval cell fate, we demonstrate that fate specification

23 and smo-1, the gene encoding SUMO-1, inhibit vulval cell fates and function at the level of lin-1, in

24 Genetic studies showed that mep-1 inhibits vulval cell fates and functions at the level of lin-1.

25 NURF-like complex promotes the expression of vulval cell fates by antagonizing the transcriptional an

26 by screening for suppressors of the ectopic vulval cell fates caused by a gain-of-function mutation

27 signaling is necessary for the induction of vulval cell fates during Caenorhabditis elegans developm

28 The LIN-1 ETS transcription factor inhibits vulval cell fates during Caenorhabditis elegans developm

29 gnaling pathways cooperate to induce P12 and vulval cell fates in a Hox-dependent manner.

30 tly to negatively regulate the expression of vulval cell fates in Caenorhabditis elegans.

31 confer a precise spatial pattern of distinct vulval cell fates in the third larval stage, a day after

32 recommender acts with lin-35 Rb to regulate vulval cell fates, and that another gene (wrm-1) acts an

33 dundantly to antagonize the specification of vulval cell fates, which are promoted by an RTK/Ras path

34 hat sumoylation promotes LIN-1 inhibition of vulval cell fates.

35 that cgr-1 positively regulates induction of vulval cell fates.

36 scriptional repression of genes that promote vulval cell fates.

37 unctions in a parallel pathway that promotes vulval cell fates.

38 cgr-1 functions cell autonomously to affect vulval cell fates.

39 ys an important role in the determination of vulval cell fates.

40 l viability, fertility, and the induction of vulval cell fates.

41 to multiple classes that redundantly inhibit vulval cell fates.

42 en FGF and Wnt in C. elegans development and vulval cell lineage polarity, and highlight the promiscu

43 rter constructs are expressed dynamically in vulval cell lineages.

44 and mig-2 are also redundantly required for vulval cell migrations and play a minor role in vulval f

45 nitially utilized the Caenorhabditis elegans vulval cell model, an in vivo system developed to study

46 cis-regulatory regions sufficient to confer vulval cell type-specific regulation when fused in cis t

47 the regulatory network architecture for each vulval cell type.

48 During the fourth larval stage (L4), seven vulval cell types are produced, each of which executes a

49 how such pathways interact to specify unique vulval cell types in a precise pattern, we have identifi

50 This pattern of vulval cell types is likely to depend on the cis-regulat

51 gulate target gene expression in the diverse vulval cell types.

52 in egl-26 mutant animals are normal, but one vulval cell, vulF, adopts an abnormal morphology.

53 for forming the toroidal shape of the dorsal vulval cell, vulF.

54 ic Multivulval (SynMuv) genes in controlling vulval cell-fate adoption.

55 emodeling activities negatively regulate the vulval cell-fate decision, we isolated a suppressor of t

56 ly with both the A and B classes of genes in vulval cell-fate determination.

57 ed met-1 and met-2 as negative regulators of vulval cell-fate specification.

58 e organs is always bounded by a non-dividing vulval cell.

59 l-17, zmp-1, and cdh-3 promote expression in vulval cells and the anchor cell (AC).

60 es in C. elegans including the ingression of vulval cells as well as germline proliferation.

61 7::GFP reporter gene in primary or secondary vulval cells at certain stages were identified.

62 amatically increased in a specific subset of vulval cells during vulval morphogenesis.

63 itis elegans, we show that actively dividing vulval cells facilitate enlargement of this breach by pr

64 In the absence of lin-11 function, vulval cells fail to acquire correct identity and inappr

65 we show that lin-11 is initially required in vulval cells for establishing the correct invagination p

66 onic acid production in a specific subset of vulval cells helps determine the shape of the vulva.

67 We examined the fate of vulval cells in lin-11 mutant animals using five cellula

68 Expression in the primary vulval cells is correlated with the precise positioning

69 sequences drive expression in glial-like and vulval cells, and that ADT-2 activity is required for no

70 l extends cellular processes normally toward vulval cells, but these processes fail to remove the bas

71 es increased integrin levels in non-dividing vulval cells, stabilizing gap position.

72 rval lethality by expression of ELT-6 in non-vulval cells, the post-embryonic cells (P3.p-P8.p) that

73 pattern of a subset of the 2 degrees lineage vulval cells.

74 e pi cell fate, crucial for a proper uterine-vulval connection and egg laying.

75 nad, the anchor cell (AC), initiates uterine-vulval contact through a cell invasion event.

76 xpression of egl-18 can partially rescue the vulval defects caused by reduced lin-39 activity.

77 ominant-negative mutant forms of mig-2 cause vulval defects that are very similar to those seen in ce

78 egl-18 mutations do not complement nT1 for vulval defects, and the nT1 breakpoint on LGIV is locate

79 ne nucleotide exchange factor) cause similar vulval defects, suggesting that UNC-73 is an exchange fa

80 epidermal growth factor-like receptors to a vulval-derived LIN-3 EGF signal and adopt the uterine vu

81 ulval-uterine coordination due to precocious vulval development also leads to uv1 cell differentiatio

82 ene, which plays a role in gonadogenesis and vulval development and encodes a Notch ligand, is derepr

83 rstanding of how these genes function during vulval development and have also identified roles for th

84 The hda-1(cw2) mutation causes defective vulval development and reduced fertility, like hda-1(e17

85 ns as heterochronic regulators of larval and vulval development but have recently been implicated in

86 Studies of C. elegans vulval development have illuminated mechanisms underlyin

87 Ras-mediated vulval development in C. elegans is inhibited by the fun

88 s (VPCs) by LIN-3/EGF from the gonad induces vulval development in C. elegans.

89 To illustrate, a geometric model fit to vulval development in Caenorhabditis elegans, implies a

90 During vulval development in Caenorhabditis elegans, six precur

91 al for viability, seam cell development, and vulval development in Caenorhabditis elegans.

92 Vulval development in Caenorhabiditis elegans is inhibit

93 Vulval development in the nematode Caenorhabditis elegan

94 Vulval development in the nematode Caenorhabiditis elega

95 Caenorhabditis elegans vulval development is a paradigmatic example of animal o

96 The vulval development of Caenorhabditis elegans provides an

97 A recent study of Caenorhabditis elegans vulval development reports a novel invasive mechanism in

98 signaling network underlying Caenorhabditis vulval development specifies three fates in a row of six

99 obtain cell-cycle statistics for C. elegans vulval development, a paradigm for organogenesis.

100 legans ROR homolog, cam-1, during C. elegans vulval development, a Wnt-regulated process.

101 During Caenorhabditis elegans vulval development, activation of receptor tyrosine kina

102 ated MAGUK in Caenorhabditis elegans, blocks vulval development, and mutation of the postsynaptic den

103 NuRD-like complex and HP1 homologs regulate vulval development, but no HMT is known to act in this p

104 ur results suggest that in the inhibition of vulval development, homologs of SETDB1, HP1 and the NuRD

105 lass B synMuv genes act together to regulate vulval development, lin-61 functions separately from som

106 During C. elegans vulval development, the anchor cell (AC) in the somatic

107 network topology for cell patterning during vulval development, we developed a mathematical model of

108 utations of the same class undergo wild-type vulval development, whereas animals with mutations of an

109 erus is not due to precocious or accelerated vulval development.

110 parallel to LIN-17/Frizzled (Fz) during worm vulval development.

111 as signaling pathway that induces C. elegans vulval development.

112 mote cell proliferation at multiple steps of vulval development.

113 onstrate multiple functions of lin-11 during vulval development.

114 iptional targets of intercellular signals in vulval development.

115 scription in the AC and thus are involved in vulval development.

116 he AC must be precisely regulated for proper vulval development.

117 c postembryonic defects in gonadogenesis and vulval development.

118 /Notch pathway during Caenorhabditis elegans vulval development.

119 e role of Rac signaling during each phase of vulval development.

120 ific to the role of LIN-35 in intestinal and vulval development.

121 in-3 EGF to negatively regulate Ras-mediated vulval development.

122 /MAPK by the inductive signal that initiates vulval development.

123 dentify attenuators of RAS signalling during vulval development.

124 at the O. tipulae cov-3 locus, which affect vulval development.

125 s fos-1 has been shown to act in uterine and vulval development.

126 required for neuronal migrations and during vulval development.

127 of let-7 results in irregular hypodermal and vulval development.

128 lin-3, which encodes the signal that induces vulval development.

129 gonad, the critical organizer of uterine and vulval development.

130 fications converge to inhibit Ras-stimulated vulval development: sumoylation, histone tail deacetylat

131 Cel-mig-13 mutants also have an unsuspected vulval-development phenotype.

132 Vulval differentiation in Caenorhabditis elegans is cont

133 n cellular migration, neuronal function, and vulval differentiation, consistent with their known role

134 dimers bind two consensus HOX/PBC sites in a vulval enhancer region of egl-18/elt-6, one of which is

135 prevents the protein from functioning in the vulval epithelia but does not prevent it from functionin

136 o not prevent LIN-10 from functioning in the vulval epithelia.

137 SYG-2 is expressed transiently by primary vulval epithelial cells during synapse formation.

138 Instead, vulval epithelial cells that contact HSNL act as synapti

139 llular processes, such as differentiation of vulval epithelial cells, function of chemosensory neuron

140 ion that resemble those in animals that lack vulval epithelial cells: HSNL synaptic vesicles fail to

141 Synaptic guidepost cells in the C. elegans vulval epithelium drive synapses from the HSNL motor neu

142 process during anchor-cell invasion into the vulval epithelium in C. elegans.

143 more than 20%, displacing surrounding BM and vulval epithelium.

144 ment membranes separating the gonad from the vulval epithelium.

145 ion of LIN-3 (EGF) and then invades into the vulval epithelium.

146 350-bp cis-regulatory region sufficient for vulval expression just upstream of the nT1 breakpoint.

147 egl-18/elt-6, one of which is essential for vulval expression of egl-18/elt-6 reporter constructs.

148 itis elegans sqv (squashed vulva) genes, the vulval extracellular space fails to expand during vulval

149 time that let-60/RAS specifies the 1 degrees vulval fate in that cell, and mir-84 overexpression supp

150 alization of the AMPAR subunit GLR-1 and for vulval fate induction in epithelia.

151 ence that DPY-22 also inhibits RAS-dependent vulval fate specification independently of BAR-1, and pr

152 val cell migrations and play a minor role in vulval fate specification.

153 signalling to prevent erroneous adoption of vulval fate.

154 LIN-35 Rb may inhibit vulval fates by regulating a signal from hyp7 to the VPC

155 e existence of a novel pathway for promoting vulval fates in C. elegans that involves activation of t

156 precursor cells (VPCs) are induced to adopt vulval fates in the third larval stage by LIN-3, an EGF-

157 ell generates the LIN-3/EGF ligand to induce vulval fates in the underlying hypodermis, whereas FBF,

158 3, and FBF act in the germ line to influence vulval fates.

159 mal syncytium and not in the VPCs to inhibit vulval fates.

160 receptor-Ras-MAP kinase pathway that promote vulval fates.

161 bility of activated LET-23 to induce ectopic vulval fates.

162 y screening for hermaphrodites with abnormal vulval formation or germline function.

163 ation of evl-20 function results in abnormal vulval, gonad, and male tail development and disrupts em

164 reens, we identified novel components of the vulval GRN, including nhr-113 in vulA.

165 by the AC response to this cue, as well as a vulval-independent mechanism that weakly drives invasion

166 by sur-6, positively regulates Ras-mediated vulval induction and acts at a step between Ras and Raf.

167 the kinase PAR-1 as a negative regulator of vulval induction and show that it acts in opposition to

168 (MAPK) signaling pathway plays a key role in vulval induction in Caenorhabditis elegans.

169 tercellular signaling system responsible for vulval induction in Caenorhabditis elegans.

170 e identify H37N21.1 as a gene that regulates vulval induction in let-60(n1046gf), a strain with a gai

171 nMuv) genes negatively regulate Ras-mediated vulval induction in the nematode Caenorhabditis elegans.

172 This pathway is not essential for vulval induction on standard Petri plates, but can be st

173 thesis that the class A synMuv genes control vulval induction through the transcriptional regulation

174 The learned model is capable of simulating vulval induction under 36 different genetic conditions.

175 During vulval induction, each of the six multipotent vulval pre

176 is similar in all six VPCs before and after vulval induction, suggesting that relief of LIN-1-mediat

177 cy exists in Wnt signaling during C. elegans vulval induction.

178 encoded by let-92, also positively regulates vulval induction.

179 repress transcription of genes required for vulval induction.

180 may play an important role during C. elegans vulval induction.

181 promotes or maintains VPC competence before vulval induction.

182 redundantly with FOG-1 and FOG-3 to control vulval induction: animals lacking FBF and either FOG-1 o

183 rnatives to surgery for female patients with vulval intraepithelial neoplasia after exclusion of occu

184 active, safe, and feasible for treatment of vulval intraepithelial neoplasia and warrant further inv

185 Eligibility criteria were biopsy-proven vulval intraepithelial neoplasia grade 3 and at least on

186 Vulval intraepithelial neoplasia is a skin disorder affe

187 ly, the standard treatment for patients with vulval intraepithelial neoplasia is surgery, but this ap

188 ternative to surgery in female patients with vulval intraepithelial neoplasia.

189 ll, a defect analogous to that of incomplete vulval invagination.

190 ng defective because of the abnormalities in vulval lineage and uterine seam-cell formation.

191 is predominantly stimulated by the 1 degrees vulval lineage cells, which generate a diffusible signal

192 processes between the two central 1 degrees vulval lineage cells.

193 t egl-26 activity is required in the primary vulval lineage for vulF morphogenesis.

194 GL-26 to GFP was observed within the primary vulval lineage only in vulE, which neighbors vulF.

195 the anterior/posterior polarity of the P7.p vulval lineage, and mutations in lin-17/Frizzled cause l

196 ryonic cell divisions including those of the vulval lineage.

197 n-18 affect cell fate patterning in the P7.p vulval lineage.

198 We demonstrate that vulval lineages in egl-26 mutant animals are normal, but

199 cause novel phenotypes in late patterning in vulval lineages, establishment of the vulva-uterine conn

200 eveloping vulF toroid is required for dorsal vulval lumen formation to complete vulval tubulogenesis.

201 pends on the LIN-12/Notch signaling, while a vulval module depends on the LIN-17-mediated Wnt signali

202 lva and in oocytes, where they likely act in vulval morphogenesis and embryonic development, respecti

203 egans sqv (squashed vulva) genes affect both vulval morphogenesis and embryonic development.

204 strongly support a model in which C. elegans vulval morphogenesis and zygotic cytokinesis depend on t

205 s in cytokinesis during embryogenesis and in vulval morphogenesis during postembryonic development.

206 Vulval morphogenesis in Caenorhabditis elegans generates

207 s sqv-3, -7, and -8, which are necessary for vulval morphogenesis in Caenorhabditis elegans, affect t

208 Caenorhabditis elegans mutants defective in vulval morphogenesis, we isolated multiple mutants in wh

209 essential roles in embryonic development and vulval morphogenesis.

210 physically with LIN-11, and is necessary for vulval morphogenesis.

211 RNAi approach, we show that lin-11 regulates vulval morphogenesis.

212 l extracellular space fails to expand during vulval morphogenesis.

213 urface composition, or cell signaling during vulval morphogenesis.

214 in a specific subset of vulval cells during vulval morphogenesis.

215 lying abnormal cell fusion causing defective vulval morphology in mutant worms.

216 -associated neurons (CANs) disrupts mid-body vulval morphology, and produces ectopic vulval tissue in

217 olog egl-30 blocked serotonin stimulation of vulval muscle Ca(2+) transients, while mutations in the

218 es, as expression occurs in both uterine and vulval muscle precursors.

219 and mpz-1 overlap in 3 pairs of neurons and vulval muscle.

220 nimals and is rescued by ser-1 expression in vulval muscle.

221 including the MC, M2, M3, M4, and M5, and in vulval muscle.

222 subunit genes altered the responses of both vulval muscles and egg-laying neurons to serotonin; spec

223 ng behavior through direct excitation of the vulval muscles and VC motor neurons.

224 The vulval muscles do not function in the presence of elevat

225 ctions both in the nervous system and in the vulval muscles for egg-laying behavior.

226 we found that serotonin acts directly on the vulval muscles to increase the frequency of Ca(2+) trans

227 role in the egg-laying circuit, exciting the vulval muscles while feedback-inhibiting the HSNs.

228 myoblasts (SMs), which generate uterine and vulval muscles, cause defects in utse morphology.

229 ressed in about 60 neurons and body wall and vulval muscles.

230 ectly modulating the functional state of the vulval muscles.

231 cZ reporter protein limited to body-wall and vulval muscles.

232 eir normal fates, instead differentiating as vulval muscles.

233 ng body wall muscles, pharyngeal muscles and vulval muscles.

234 nervates its major postsynaptic targets, the vulval muscles.

235 served sequences necessary for expression in vulval or seam cells.

236 es Aikens and colleagues showed that chronic vulval pain (vulvodynia or vulvar dysaesthesia) is assoc

237 better understanding of the pathogenesis of vulval pain and how to manage it appropriately.

238 d a useful approach to patients with chronic vulval pain.

239 fate plasticity during dauer and for normal vulval patterning after passage through dauer, suggestin

240 ive tunings of this same network can explain vulval patterning observed experimentally in C. elegans,

241 ation of lin-11 is crucial for the wild-type vulval patterning.

242 Here we present evidence that the nT1 vulval phenotype is due to a disruption of egl-18/elt-6

243 Unc) phenotype of bar-1 mutants, but not the vulval phenotype, suggesting that a Wnt pathway may act

244 In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the act

245 s LIN-12/Notch during Caenorhabditis elegans vulval precursor cell (VPC) fate patterning.

246 Specification of vulval precursor cell (VPC) fates in C. elegans has serv

247 The source of the FGF ligand is the primary vulval precursor cell (VPC) P6.p, which controls the ori

248 el of LIN-3/LIN-12-mediated signaling in the vulval precursor cell array.

249 uch as interspecific differences in isolated vulval precursor cell behavior and in spatial regulation

250 Two seemingly conflicting verbal models of vulval precursor cell fate specification have been propo

251 a let-7 family member, is largely absent in vulval precursor cell P6.p at the time that let-60/RAS s

252 t-grandprogeny of the Caenorhabditis elegans vulval precursor cells (VPCs) adopt one of the final vul

253 cesses, including cell fate specification by vulval precursor cells (VPCs) and migration of the Q(L)

254 vating the EGF receptor signaling pathway in vulval precursor cells (VPCs) and thereby inducing and p

255 Vulval precursor cells (VPCs) are induced to adopt vulva

256 Six vulval precursor cells (VPCs) are initially equivalent b

257 The vulval precursor cells (VPCs) are spatially patterned by

258 The vulval precursor cells (VPCs) are spatially patterned du

259 Activation of EGFR-Ras-MAPK signaling in vulval precursor cells (VPCs) by LIN-3/EGF from the gona

260 ulval induction, each of the six multipotent vulval precursor cells (VPCs) commits to one of three fa

261 by the opposite division orientation of the vulval precursor cells (VPCs) flanking the axis of symme

262 ays occurs during the patterning of a row of vulval precursor cells (VPCs) in Caenorhabditis elegans:

263 The vulval precursor cells (VPCs) of Caenorhabditis elegans

264 The Caenorhabditis elegans vulval precursor cells (VPCs) offer a paradigm for inves

265 ling pathways specify Caenorhabditis elegans vulval precursor cells (VPCs) to adopt a spatial pattern

266 as and Notch signaling pathways causes three vulval precursor cells (VPCs) to adopt induced cell fate

267 stem, cells that give rise to the vulva, the vulval precursor cells (VPCs), remain quiescent for two

268 hat has similar developmental origins to the vulval precursor cells (VPCs), which generate the vulva

269 hat generate ventral cord neurons (VCNs) and vulval precursor cells (VPCs).

270 notype is generated by aberrant induction of vulval precursor cells (VPCs): in wild-type animals, thr

271 The fates of six vulval precursor cells are patterned through the action

272 Moreover, 2 degrees vulval precursor cells occasionally adopt the 3 degrees

273 yonic cells (P3.p-P8.p) that normally become vulval precursor cells often fuse with the surrounding e

274 tissue in multivulva animals is generated by vulval precursor cells that in the wild type do not gene

275 Analysis of ERK activity over time in the vulval precursor cells, a well-characterized paradigm of

276 In a subset of Pn.p cells, called vulval precursor cells, nhr-25 acts collaboratively with

277 FP fusion gene is expressed in many neurons, vulval precursor cells, the distal tip cell (DTC), intes

278 sterior axis and 6 of these cells become the vulval precursor cells.

279 sues examined, including polarised growth of vulval precursors and seam cells, migrations of neurobla

280 somi-1 inhibits lin-14 and induction of the vulval precursors by the let-60/RAS pathway.

281 red to regulate cell fates and fusion in the vulval primordium and are essential to form a vulva.

282 nd receptor function in another Wnt-mediated vulval process, the orientation of the P7.p lineage.

283 in addition to its canonical effector, Raf, vulval Ras utilizes an exchange factor for the Ral small

284 rmore has no serotonin-IR innervation of the vulval region, in contrast to every other species we exa

285 The cells that normally form the ventral vulval rings fail to make contact or adhere and conseque

286 this process by experimentally modifying key vulval signaling pathways in different species of Caenor

287 This factor also stimulates the vulval slit to widen, so that the male copulatory spicul

288 associate in a nuclear complex that inhibits vulval specification by repressing lin-3 EGF expression.

289 been proposed to silence genes required for vulval specification through chromatin modification and

290 in formation of an abnormally thick layer of vulval tissue at the apex of the vulva and a physical bl

291 The ectopic vulval tissue in multivulva animals is generated by vulv

292 body vulval morphology, and produces ectopic vulval tissue in the posterior epidermis, in a Wnt-depen

293 cells that in the wild type do not generate vulval tissue.

294 that expands the breach and crosses into the vulval tissue.

295 P-29 to form a large protrusion that invades vulval tissue.

296 or dorsal vulval lumen formation to complete vulval tubulogenesis.

297 ifying fate, the AC directly promotes dorsal vulval tubulogenesis.

298 smo-1 animals lack a vulval-uterine connection as a result of impaired ventra

299 ssociated with the formation of a functional vulval-uterine connection.

300 t of this model, we demonstrate that lack of vulval-uterine coordination due to precocious vulval dev