ライフサイエンスコーパス: epiblast

1 how similarity to pre-gastrulation formative epiblast.

2 ylation, intermediate between early and late epiblast.

3 tation epiblast and are distinct from primed epiblast.

4 cyst: trophectoderm, primitive endoderm, and epiblast.

5 priming to enhance the developing embryonic epiblast.

6 iptional output and development of the mouse epiblast.

7 hich establishes neural fate in the anterior epiblast.

8 differentiation in cultured cells and native epiblast.

9 D4 and TDGF1, are also enriched in the human epiblast.

10 ain the distinctly rapid growth of the mouse epiblast.

11 l circuitry operative in the preimplantation epiblast.

12 itive streak on axial progenitors within the epiblast.

13 closely recapitulates the pluripotent naive epiblast.

14 it is programmed cell death that shapes the epiblast.

15 on events taking place in the gastrula stage epiblast.

16 ntrolling apoptosis in the post-implantation epiblast.

17 ell lines equivalent to the postimplantation epiblast.

18 erm and soon after in the adjacent posterior epiblast.

19 widespread FGF/MAPK activity in the gastrula epiblast.

20 ndent apoptosis specifically in the E3.5-4.5 epiblast.

21 actions between this layer and the subjacent epiblast.

22 otes mesodermal development in the posterior epiblast.

23 gher than in junctions of other cells in the epiblast.

24 pite being expressed in the postimplantation epiblast.

25 ilenced by bi-allelic DNA methylation in the epiblast.

26 Cs) share features with the pre-implantation epiblast.

27 s, we derive stem cells from formative mouse epiblast.

28 ive pluripotency and cell competition in the epiblast.

29 conversion from naive to primed state of the epiblast.

30 al cells is already established in the early epiblast.

31 ssioning of enhancers activated in formative epiblast.

32 ncy in primed cells of the post-implantation epiblast.

33 ene expression are similar to a day 10 human epiblast.

34 c cell fate decisions in the early posterior epiblast.

35 mally expressed in the pregastrulation stage epiblast.

36 males is attained via X-inactivation in late epiblasts.

37 Moreover, they show that epiblast-ablated embryos can be used to test the potency

38 Embryos with an epiblast ablation of Aurora A properly establish the ant

39 e the transcriptome of the post-implantation epiblast and all PGC stages in rat to reveal enrichment

40 fashion, landmarks of the development of the epiblast and amniotic ectoderm parts of the conceptus, i

41 display features of early post-implantation epiblast and are distinct from primed epiblast.

42 lacental trophoblast (TB) that surrounds the epiblast and associated embryonic tissues during the eni

43 anized fate specification in differentiating epiblast and ectodermal tissues.

44 em cells (ESCs) resemble the preimplantation epiblast and efficiently contribute to chimaeras.

45 hibition of ESC differentiation towards both epiblast and endoderm lineages.

46 ntify imprinted regions in post-implantation epiblast and extra-embryonic ectoderm (ExE) by assaying

47 Upon implantation, the epiblast and extraembryonic ectoderm of the mouse embryo

48 nes defining differentiation programs in the epiblast and extraembryonic ectoderm.

49 mouse preimplantation embryo into the early epiblast and extraembryonic ectoderm.

50 d trophectoderm in early blastocysts, and of epiblast and hypoblast in late blastocysts.

51 ng preimplantation development: trophoblast, epiblast and hypoblast.

52 egulate pluripotency in the pre-implantation epiblast and in derivative embryonic stem cells.

53 en cycle of pluripotency, naive in the early epiblast and latent in the germline, that is sustained b

54 Here, using chicken epiblast and mammalian pluripotency stem cell (PSC) mode

55 Here we analyse 1,205 cells from the epiblast and nascent Flk1(+) mesoderm of gastrulating mo

56 oincide directly with lineage restriction of epiblast and PrE markers, but rather with exclusion of t

57 r for PrE, we investigated the plasticity of epiblast and PrE precursors.

58 KC as a central player in the segregation of epiblast and PrE progenitors in the mouse blastocyst.

59 marker expression during the segregation of epiblast and PrE within the ICM.

60 We identified in silico precursors of the epiblast and primitive endoderm lineages and revealed a

61 We show that a consistent ratio of epiblast and primitive endoderm lineages is achieved thr

62 participate in the communication between the epiblast and the extraembryonic ectoderm (ExE) of the de

63 directed by cross talk between the embryonic epiblast and the first extra-embryonic tissue, the troph

64 al landmarks, including lumenogenesis of the epiblast and the resultant pro-amniotic cavity, formatio

65 he conceptus, including lumenogenesis of the epiblast and the resultant pro-amniotic cavity, formatio

66 re we investigated the crosstalk between the epiblast and the trophectoderm (TE) during pig embryo el

67 The crosstalk between the epiblast and the trophoblast is critical in supporting t

68 s (ICM), which gives rise to the pluripotent epiblast and therefore the future embryo, and the trophe

69 Mettl3 knockout preimplantation epiblasts and naive embryonic stem cells are depleted fo

70 ivated ahead of other Nodal enhancers in the epiblast, and is essential to Nodal expression in embryo

71 n is crucial for the transition of ESCs into epiblast, and the methyltransferase-like protein Dnmt3l,

72 However, the mechanisms underlying epiblast apoptosis are unclear.

73 hat embryos lacking Wnt3 specifically in the epiblast are able to initiate gastrulation and advance t

74 ression signatures of dKO ESCs and diapaused epiblasts are remarkably similar.

75 ent stem cells (hPSC) resemble the embryonic epiblast at an earlier time-point in development than co

76 mbryo, E-cadherin is weakly expressed in the epiblast at pre-primitive streak stages where it is subs

77 ial to mesenchymal transition on a subset of epiblast axial progenitors.

78 rved first and switches to random XCI in the epiblast but not placental lineages.

79 ryo environment restricts the fate choice of epiblast but not PrE precursors, thus ensuring the forma

80 is initially expressed broadly in the entire epiblast, but becomes gradually restricted as cell fates

81 ells in the posterior-proximal region of the epiblast, but the mechanisms that specify primitive bloo

82 te from specific regions of the pre-gastrula epiblast, but the plasticity of cells within the embryo

83 the posterior pre-primitive-streak competent epiblast by sequential upregulation of SOX17 and BLIMP1

84 Our work demonstrates that a model human epiblast can break axial symmetry despite the absence of

85 bearing resemblance to preimplantation mouse epiblasts, can be established through dual inhibition (2

86 polar trophoblast signaling is prevented via epiblast cavitation which leads to the (pro)amniotic cav

87 a role in fixing the body plan: it controls epiblast cell movements leading to primitive streak form

88 Because X(DeltaTsix)X female embryonic epiblast cells and EpiSCs harbor an inactivated X chromo

89 n signaling that coordinates polarization of epiblast cells and their apical constriction, a prerequi

90 during differentiation of embryonic stem to epiblast cells and uncovered the forkhead transcription

91 During gastrulation, epiblast cells are pluripotent and their fate is thought

92 In mouse embryo gastrulation, epiblast cells delaminate at the primitive streak to for

93 descendants of these two lineages, in which epiblast cells differentiate into endoderm at two distin

94 rtion locally, and thereby the transmigrated epiblast cells emerge as the DVE cells.

95 ll levels of ERK activity, while pluripotent epiblast cells exhibited lower basal activity with spora

96 l stage, continuing through the emergence of epiblast cells in preimplantation blastocysts, and ceasi

97 ds to ribosomal DNA, and that both Chd1(-/-) epiblast cells in vivo and ESCs in vitro express signifi

98 Transformation of pluripotent epiblast cells into a cup-shaped epithelium as the mouse

99 initiates the differentiation of pluripotent epiblast cells into germ layers.

100 Later, around implantation, epiblast cells of the inner cell mass that give rise to

101 GCLCs) mimics the in vivo differentiation of epiblast cells to PGCs, how DNA methylation status of PG

102 Following implantation, mouse epiblast cells transit from a naive to a primed state in

103 Concomitantly, epiblast cells transit through distinct pluripotent stat

104 It is critical that epiblast cells within blastocyst-stage embryos receive t

105 pecific cells within the early embryo (e.g., epiblast cells) and of certain cells propagated in vitro

106 gnalling abrogates NANOG expression in human epiblast cells, consistent with a requirement for this p

107 It is a unique feature of embryonic epiblast cells, existing only transiently, as cells pass

108 In epiblast cells, TET1 demethylates gene promoters via hyd

109 ght a potential regulatory mechanism whereby epiblast cells, via their shed EVs, create an environmen

110 ns in rapidly proliferating postimplantation epiblast cells.

111 of pluripotency in human embryonic stem and epiblast cells.

112 ithout inducing premature differentiation of epiblast cells.

113 lopmental potential relative to primed mouse epiblast cells.

114 ring PGC specification from postimplantation epiblast cells.

115 and to exhibit properties characteristic of epiblast cells.

116 derm differentiation and causes apoptosis of epiblast cells.

117 The relationship between epiblast cellular morphology and its pluripotency is not

118 The mammalian embryo's caudal lateral epiblast (CLE) harbours bipotent progenitors, called neu

119 regulated in the primitive streak and in the epiblast, concomitant with the formation of mesendoderma

120 Mouse embryonic stem cells derived from the epiblast contribute to the somatic lineages and the germ

121 we report that Zic3 is primarily required in epiblast derivatives to affect left-right patterning and

122 Selective Grhl2 inactivation only in epiblast-derived cells rescued all placental defects but

123 prevent JAK/STAT3 induced post-implantation epiblast-derived stem cell conversion into naive pluripo

124 Mouse embryonic stem cells (ESCs) and epiblast-derived stem cells (EpiSCs) represent the initi

125 of ES cells, and is sufficient to reprogram epiblast-derived stem cells to naive pluripotency in ser

126 We also show that reprogramming of epiblast-derived stem cells to naive pluripotency requir

127 elopment to show the conserved principles of epiblast development for competency for primordial germ

128 an naive cells tracks the progression of the epiblast during embryogenesis in Macaca fascicularis, bu

129 required within the prospective neural crest epiblast during gastrulation and is unlikely to operate

130 hment of the primitive endoderm layer to the epiblast during the formation of a basement membrane, a

131 s contain cells transcriptionally similar to epiblast, ectoderm, mesoderm, endoderm, primordial germ

132 ctive in integrin adhesion complex assembly, epiblast elongation, and lineage differentiation.

133 s representing the inner cell mass (ICM) and epiblast embryos.

134 d at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlli

135 Formation of epiblast (EPI) - the founder line of all embryonic linea

136 The emergence of pluripotent epiblast (EPI) and primitive endoderm (PrE) lineages wit

137 an inner cell mass comprising two lineages: epiblast (Epi) and primitive endoderm (PrE).

138 they are derived, contain precursors of the epiblast (Epi) and primitive endoderm (PrEn) lineages.

139 n in the context of the decision between the epiblast (Epi) and the primitive endoderm (PrE) fate tha

140 ping blastocyst: the trophectoderm (TE), the epiblast (Epi) and the primitive endoderm (PrE).

141 gulates establishment of pluripotency in the epiblast (EPI) have not been fully elucidated.

142 m (TE) or inner cell mass (ICM), followed by epiblast (EPI) or primitive endoderm (PE) specification

143 he inner cell mass (ICM) can be specified in epiblast (Epi) or primitive endoderm (PrE).

144 Around implantation, the epiblast (Epi) transits from naive to primed pluripotenc

145 primitive endoderm (PrE) versus pluripotent epiblast (EPI) within the inner cell mass (ICM) of the m

146 use blastocyst gives rise to the pluripotent epiblast (EPI), which forms the embryo proper, and the p

147 s within the inner cell mass to generate the epiblast (EPI), which will form the new organism, from t

148 ll mass (ICM) to primitive endoderm (PE) and epiblast (EPI).

149 protein phosphatase activity is required for epiblast epithelial differentiation and polarization.

150 cted naive pluripotent state is required for epiblast epithelialization and generation of the pro-amn

151 ar pluripotent stem cells into the polarized epiblast epithelium.

152 y landmarks of normal development, including epiblast expansion, lineage segregation, bi-laminar disc

153 vealed a role for MCRS1, TET1, and THAP11 in epiblast formation and their ability to induce naive plu

154 y, whose function is to distance the central epiblast from such signaling interactions.

155 the area of pluripotency maintenance in the epiblast from which the mESCs are derived.

156 Similarly, exit of epiblasts from naive pluripotency in cultured human post

157 erentiation starts at gastrulation, when the epiblast generates mesoderm and endoderm germ layers thr

158 The pluripotent epiblast gives rise to all tissues and organs in the adu

159 Explants of this epiblast grown in the absence of further signals develop

160 or primed pluripotency but rather stabilizes epiblast identity during the transition between these st

161 tate is inherently linked to preimplantation epiblast identity in the embryo.

162 The polar trophoblast overlays the epiblast in eutherian mammals and, depending on the spec

163 further established in the peri-implantation epiblast in vivo.

164 developmental progression of the pluripotent epiblast in vivo.

165 esults in ectopic BMP signaling in the mouse epiblast in vivo.

166 e of E8 hPSCs and the pre-implantation human epiblast in vivo.

167 anscriptome signatures akin to the diapaused epiblasts in vivo.

168 Conversely, unlike the epiblast, in which XCI is not required for progenitor ce

169 , but also for regulators of the pluripotent epiblast, including NANOG.

170 clusively expressed in the human pluripotent epiblast, including the transcription factor KLF17.

171 morphogenetic event transforms the amorphous epiblast into a rosette of polarized cells.

172 nal tension of mesendoderm precursors in the epiblast is higher in junctions oriented in the directio

173 left-right patterning and its expression in epiblast is necessary for proper transcriptional control

174 Injection of ES cells into Aurora A epiblast knockout blastocysts reconstitutes embryonic de

175 hereas the homozygous deletion in the entire epiblast leads to pancreas agenesis associated with abno

176 rowth factor (bFGF) and activin A develop as epiblast-like cells (EpiLCs) and gain competence for a P

177 naive embryonic stem cells (ESCs) and primed epiblast-like cells (EpiLCs).

178 id de novo DNA methylation during priming to epiblast-like cells, methylation is globally erased in P

179 ctivated and poised enhancers in ESC-derived epiblast-like cells.

180 o-basal polarity is critical for the lumenal epiblast-like morphogenesis of human pluripotent stem ce

181 a tankyrase inhibitor-regulated human naive epiblast-like pluripotent state.

182 ion is stalled at an early post-implantation epiblast-like stage, while Jmjd2c-knockout ESCs remain c

183 s them to self-organize and form the lumenal epiblast-like stage.

184 ation and its sister pluripotent (embryonic) epiblast lineage.

185 tories of primitive endoderm, trophectoderm, epiblast lineages, and PGCLCs.

186 to embryogenesis but contribute primarily to epiblast lineages.

187 expression of pluripotency marker (Oct4) and epiblast marker (Fgf5) and decreased expression of linea

188 Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, t

189 Use of an in vitro model of epiblast maturation, relying on the differentiation of E

190 gnificant for priming differentiation during epiblast maturation.

191 postimplantation development by facilitating epiblast maturation.

192 m the egg; in mice, Blimp1 expression in the epiblast mediates the commitment of cells to the germ li

193 Epiblast MET and its subsequent EMT are two distinct pro

194 Reintroduction of Myo/Nog cells into the epiblast of ablated embryos restores normal patterns of

195 in various locations and orientations in the epiblast of chick embryos in the early stages of primiti

196 the conditional inactivation of Wnt3 in the epiblast of developing mouse embryos.

197 cells survived and were integrated into the epiblast of egg-cylinder-stage embryos.

198 rodent PSCs, they never integrated into the epiblast of egg-cylinder-stage embryos.

199 The caudal lateral epiblast of mammalian embryos harbours bipotent progenit

200 ipotent stem cell state corresponding to the epiblast of the diapaused blastocyst and indicate that m

201 ollowing implantation, the naive pluripotent epiblast of the mouse blastocyst generates a rosette, un

202 otent cells of the inner cell mass (ICM) and epiblast of the peri-implantation mouse embryo, but its

203 ecessary for the stem-like properties of the epiblast of the pre-gastrulation embryo and for cellular

204 n between the extra-embryonic region and the epiblast on the posterior side of the embryo undergo an

205 in the tail region or excessive apoptosis of epiblast or mesoderm cells.

206 e molecular profile characteristic of either epiblast or primitive endoderm.

207 lastocyst differentiate into the pluripotent epiblast or the primitive endoderm (PrE), marked by the

208 progenitors emerge either directly from the epiblast or through segregation within the allantoic cor

209 Inactivation of Aurora A in the epiblast or visceral endoderm layers of the conceptus le

210 We propose that epiblast partial MET is an evolutionarily conserved proc

211 al cyst with an asymmetric amniotic ectoderm-epiblast pattern that resembles the human amniotic sac.

212 cess among all amniotic vertebrates and that epiblast pluripotency is restricted to an intermediate c

213 ough gastrulation EMT coincides with loss of epiblast pluripotency, pluripotent cells in development

214 lial lineages mostly derive from independent epiblast populations, specified before gastrulation.

215 nic primitive endoderm (PrE) and pluripotent epiblast precursors are specified in the inner cell mass

216 However, epiblast precursors exhibit less plasticity than precurs

217 Although the epiblast prematurely decreases in size, we did not detec

218 ectory and transcriptional signatures of the epiblast, primitive endoderm and trophectoderm, and iden

219 e potential of individual cells in the mouse epiblast, primitive streak, and early YS.

220 mouse pre-implantation blastocyst comprises epiblast progenitor and primitive endoderm cells of whic

221 In mouse epiblast progenitors, Nodal-SMAD and RREB1 combine to in

222 This suggests that the high levels of epiblast proliferation function to move the prospective

223 ker, BRACHYURY This phenotype, and increased epiblast proliferation, arose when Rauber's layer was ma

224 ss and gain of function experiments that the epiblast provides FGF signal that results in differentia

225 esults suggest that the processes of PrE and epiblast segregation, and cell fate progression are inte

226 During gastrulation, the pluripotent epiblast self-organizes into the 3 germ layers-endoderm,

227 gastrulation, embryos that lack Pten in the epiblast show defects in the migration of mesoderm and/o

228 A functional test in differentiating epiblast shows that CDX2 and ELF5 are activated in respo

229 Here, we show that the epiblast-specific deletion of the gene encoding the BMP

230 Epiblast-specific deletion shows that Pten is not requir

231 Epiblast-specific inactivation of Cubn in the mouse embr

232 Erf epiblast-specific knockout embryos had reduced numbers o

233 anization, mimicking mtDNA bottleneck during epiblast specification.

234 onal phenotypes are distinct from effects in epiblast spheroids, indicating that they are tissue spec

235 s to protect the paternal epigenotype at the epiblast stage of development but is dispensable thereaf

236 polarized cysts, reminiscent of the lumenal epiblast stage, providing a model to explore key morphog

237 In three-dimensional cultures, epiblast-stage hPSCs form spheroids surrounding hollow,

238 n cells survived but were segregated; unlike epiblast-stage rodent PSCs, they never integrated into t

239 dermal fate while playing a required role in epiblast stem cell exit and the consequent lineage fate

240 ind that human embryonic stem cell and mouse epiblast stem cell fates are regulated by beta-catenin t

241 Its specific role in mouse epiblast stem cell self-renewal, however, remains poorly

242 Mouse embryonic stem cells (ESC) and epiblast stem cells (EpiSC) are at distinct pluripotent

243 d either from embryonic stem cells (ESCs) or epiblast stem cells (EpiSCs) and compared them with E8.2

244 similar transcriptional programs relative to epiblast stem cells (EpiSCs) and differentiated cells.

245 ics in mouse ESCs that were less frequent in epiblast stem cells (EpiSCs) and scarce in somatic tissu

246 We show that epiblast stem cells (EpiSCs) are an effective source of

247 at the Xi of mouse post-implantation-derived epiblast stem cells (EpiSCs) can be reversed by nuclear

248 However, we find that epiblast stem cells (EpiSCs) derived from the post-impla

249 irected differentiation of pluripotent mouse epiblast stem cells (EpiSCs) through defined development

250 an accelerate and enhance reversion of mouse epiblast stem cells (epiSCs) to a naive pluripotent stat

251 l-molecule inhibitor MM-401 reprograms mouse epiblast stem cells (EpiSCs) to naive pluripotency.

252 naive embryonic stem cells (ESCs) and primed epiblast stem cells (EpiSCs), and identified the constit

253 e derivation of embryonic stem cells (ESCs), epiblast stem cells (EpiSCs), and reprogramming.

254 issioning or remain constitutively active in epiblast stem cells (EpiSCs), as further established in

255 Starting from post-implantation epiblast stem cells (EpiSCs), one route advances through

256 relying on the differentiation of ESCs into epiblast stem cells (EpiSCs), revealed that this process

257 n events in vitro is possible via the use of epiblast stem cells (EpiSCs), self-renewing pluripotent

258 cription factor (TF)-dependent regulation of epiblast stem cells (EpiSCs), we performed ChIP-seq anal

259 ferentiating embryonic stem cells (ESCs) and epiblast stem cells (EpiSCs).

260 and maintenance of ESCs and postimplantation epiblast stem cells (epiSCs).

261 ouse embryonic stem cells (mESCs) and primed epiblast stem cells (mEpiSCs) represent successive snaps

262 is and maintained as embryonic stem cells or epiblast stem cells in culture.

263 Forced expression of NANOG in epiblast stem cells is sufficient to decompact chromatin

264 Human embryonic stem cells and mouse epiblast stem cells represent a primed pluripotent stem

265 molecular reprogramming of post-implantation epiblast stem cells to naive pluripotency.

266 ion, Tfcp2l1 can reprogram post-implantation epiblast stem cells to naive pluripotent ESCs.

267 ion profiling of TSCs, embryonic stem cells, epiblast stem cells, and mouse embryo fibroblasts, deriv

268 cuit in human embryonic stem cells and mouse epiblast stem cells, in which Smad2 acts through binding

269 single cell levels shows that, unlike mouse epiblast stem cells, the ESR subset of hPSC displays no

270 equivalent in developmental status to mouse epiblast stem cells, which correspond to pluripotent cel

271 an development lie in a cluster of embryonic epiblast stem cells.

272 in mouse pluripotent embryonic stem (ES) and epiblast stem cells.

273 of post-implantation development than mouse epiblast stem cells.

274 th self-renewal and differentiation in mouse epiblast stem cells.

275 ns in Xenopus ectoderm, mouse embryonic, and epiblast stem cells.

276 te, JAK/STAT3 enforces naive pluripotency in epiblast stem cells.

277 subpopulation are lower than those in mouse epiblast stem cells.

278 oactive small molecules on mouse pluripotent epiblast stem-cell-derived oligodendrocyte progenitor ce

279 Similarly, in vivo epiblasts suppress COX levels.

280 Surprisingly, TET1 represses a majority of epiblast target genes independently of methylation chang

281 tain a population of progenitor cells in the epiblast that generates mesoderm and contributes to the

282 suggest that, much like in the cells of the epiblast, the initial imprint that establishes imprinted

283 Once eliminated in the epiblast, they are neither replaced nor compensated for

284 factor PRDM1 in the orderly transition from epiblast to defined neural lineages in chick.

285 Seq) and RNA-Seq across key stages from E6.5 epiblast to E16.5 PGCs.

286 Comparison of the human epiblast to existing embryonic stem cells (hESCs) reveal

287 e for rapid progression from preimplantation epiblast to gastrulation in rodents.

288 ESCs), which are the in vitro equivalents of epiblasts, to ESC-derived extracellular vesicles (EVs) h

289 cendants of the inner cell mass in the early epiblast transit from the naive to primed pluripotent st

290 In a model of the embryonic to epiblast transition in murine stem cells, we unambiguous

291 Human pluripotent stem cells (PSCs) show epiblast-type pluripotency that is maintained with ACTIV

292 The pluripotent mammalian epiblast undergoes unusually fast cell proliferation.

293 Nanog and Gata6 are critical to specify the epiblast versus primitive endoderm (PrE) lineages.

294 in blastocyst formation and specification of epiblast versus primitive endoderm lineages using condit

295 lls arise within primitive streak-associated epiblast via a mechanism that is separable from that whi

296 uces expression of pre-neural markers in the epiblast, which also contributes to delay streak formati

297 characteristic of the multi-potent stem zone epiblast, which contains neuro-mesodermal progenitors th

298 lopment beyond implantation: the pluripotent epiblast, which generates the future embryo, and surroun

299 rentiation signals and forms the pluripotent epiblast, which gives rise to all of the tissues in the

300 in vitro three-dimensional model of a human epiblast whose size, cell polarity and gene expression a