ライフサイエンスコーパス: epiblast

1 closely recapitulates the pluripotent naive epiblast.

2 it is programmed cell death that shapes the epiblast.

3 on events taking place in the gastrula stage epiblast.

4 ntrolling apoptosis in the post-implantation epiblast.

5 ell lines equivalent to the postimplantation epiblast.

6 erm and soon after in the adjacent posterior epiblast.

7 widespread FGF/MAPK activity in the gastrula epiblast.

8 ylation, intermediate between early and late epiblast.

9 mally expressed in the pregastrulation stage epiblast.

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

11 ation, the VE is critical for patterning the epiblast.

12 oximally to genes expressed in hESCs and the epiblast.

13 tation epiblast and are distinct from primed epiblast.

14 Tgif function is required for patterning the epiblast.

15 at the surface, while deeper cells form the epiblast.

16 cyst: trophectoderm, primitive endoderm, and epiblast.

17 priming to enhance the developing embryonic epiblast.

18 iptional output and development of the mouse epiblast.

19 hich establishes neural fate in the anterior epiblast.

20 differentiation in cultured cells and native epiblast.

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

22 ain the distinctly rapid growth of the mouse epiblast.

23 l circuitry operative in the preimplantation epiblast.

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

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

26 est that talin1 binding to integrin promotes epiblast adhesion and morphogenesis in part by preventin

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

28 ial regulators of BMP signaling in the early epiblast and are indispensable for normal morphogenesis

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

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

31 Moreover, unlike epiblast and EpiSCs, rESCs contribute to somatic tissues

32 n blastocyst, which may be similar to rodent epiblast and ES cells but is not sustained during conven

33 obed directly the relationship between naive epiblast and ES cells.

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

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

36 n human blastocysts, implying segregation of epiblast and hypoblast, as in rodent embryos.

37 ng preimplantation development: trophoblast, epiblast and hypoblast.

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

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

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

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

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

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

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

45 g in intact, unmanipulated embryos until the epiblast and primitive endoderm became distinct.

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

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

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

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

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

51 on of these SoxB1 genes throughout the early epiblast and their subsequent restriction to the ectoder

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

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

54 side remain pluripotent and give rise to the epiblast, and hence the future body, whereas others deve

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

56 e distinct cell lineages: one embryonic, the epiblast, and two extraembryonic, the trophoblast and pr

57 However, the mechanisms underlying epiblast apoptosis are unclear.

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

59 at these high levels of proliferation in the epiblast are dependent on Nodal signalling and are requi

60 lines from post-implantation epithelialised epiblast are unable to colonise the embryo even though t

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

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

63 P) inhibitor noggin (Nog) are present in the epiblast before gastrulation.

64 more, chick explants isolated from embryonic epiblast behave like Xenopus animal caps and express bor

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

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

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

68 MyoD expressing cells were ablated in the epiblast by labeling them with the G8 MAb and lysing the

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

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

71 Comparison of early and late epiblast cell culture models revealed a set of early-to-

72 d the time of implantation, during which the epiblast cell cycle is uniquely structured to achieve ve

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

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

75 iSCs), which exhibit essential properties of epiblast cells and that differ from embryonic stem (ES)

76 ES cells can be derived directly from early epiblast cells and that ES cells might arise via two dif

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

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

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

80 Epiblast cells are refractory to leukaemia inhibitory fa

81 istinct small molecules [7, 8], we show that epiblast cells can become ESCs without first acquiring B

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

83 Here we show reprogramming of advanced epiblast cells from embryonic day 5.5-7.5 mouse embryos

84 or example, development of post-implantation epiblast cells from primitive ectoderm involves signific

85 d bodies (EBs) leads to massive apoptosis of epiblast cells in contact with the BM.

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

87 cells that are ex vivo counterparts of naive epiblast cells in the mature blastocyst.

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

89 because PGCs originate from postimplantation epiblast cells in vivo.

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

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

92 In addition, epiblast cells isolated from talin1-null EBs exhibit imp

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

94 Cultured epiblast cells overcome the epigenetic barrier progressi

95 that give rise to ES cells might arise from epiblast cells that are already predisposed to a primord

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

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

98 Concomitantly, epiblast cells transit through distinct pluripotent stat

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

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

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

102 roceed with the erasure of key properties of epiblast cells, resulting in DNA demethylation, X reacti

103 In epiblast cells, TET1 demethylates gene promoters via hyd

104 ithout inducing premature differentiation of epiblast cells.

105 lopmental potential relative to primed mouse epiblast cells.

106 ring PGC specification from postimplantation epiblast cells.

107 and to exhibit properties characteristic of epiblast cells.

108 derm differentiation and causes apoptosis of epiblast cells.

109 re essentially identical to pre-implantation epiblast cells.

110 loss of phenotypic and epigenetic memory of epiblast cells.

111 supplied Noggin compensated for the ablated epiblast cells.

112 ns in rapidly proliferating postimplantation epiblast cells.

113 of pluripotency in human embryonic stem and epiblast cells.

114 o, Nanog specifically demarcates the nascent epiblast, coincident with the domain of X chromosome rep

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

116 em (ES) cells derived from pluripotent early epiblast contribute functionally differentiated progeny

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

118 anterior visceral endoderm (AVE) signals to epiblast derivatives during gastrulation to orchestrate

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

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

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

122 les were significantly more aligned to mouse epiblast-derived stem cells (mEpiSCs) than to mouse ESCs

123 be readily detected in demethylated Oct4(+) epiblast-derived stem cells as well as differentiated mo

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

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

126 lated mouse embryonic stem cells (mESCs) and epiblast-derived stem cells.

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

128 use embryo that encapsulates the pluripotent epiblast distally and the extraembryonic ectoderm proxim

129 Furthermore, the epiblast does not require paracrine support from the hyp

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

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

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 cyst comprises two lineages: the pluripotent epiblast (EPI) and primitive endoderm (PrE).

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

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

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

145 primitive endoderm (PrE) and the pluripotent epiblast (EPI), the two lineages specified within the in

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

149 brane (BM) and the selective survival of the epiblast epithelium, which does.

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

151 tic double mutants display severe defects in epiblast, extraembryonic ectoderm, and anterior visceral

152 cells might be a more tractable source than epiblast for the capture of naive pluripotent stem cells

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

154 mmalian development through formation of the epiblast, founder tissue of the embryo proper.

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 primitive stem cells closely related to the epiblast/germ line.

158 at Nanog choreographs synthesis of the naive epiblast ground state in the embryo and that this functi

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

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

161 inhibitors on the development of pluripotent epiblast in intact pre-implantation embryos.

162 developmental progression of the pluripotent epiblast in vivo.

163 nt cells derived from post-implantation late epiblasts in vitro.

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

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

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

167 hese data indicate that BMP signaling in the epiblast induces Wnt3 and Wnt3a expression to maintain W

168 ablishment, as blocking cell division in the epiblast inhibits AVE migration.

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

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

171 pole of the zebrafish can be traced from the epiblast, is a discrete part of the mesodermal heart fie

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

173 ntibody to the G8 antigen was applied to the epiblast, labeled cells were later found in the ocular p

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

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

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

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

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

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

180 eveals the appearance of a transient FGF5(+) epiblast-like stage followed by PAX6(+) neural cells com

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

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

183 ew, we hypothesize that very small embryonic/epiblast-like stem cells could be a missing link that su

184 itive germ line-derived very small embryonic/epiblast-like stem cells, which are deposited early in e

185 -implantation embryo by promoting the TE and epiblast lineages while suppressing the PE lineage.

186 tes morphogenetic cell behaviors in multiple epiblast lineages.

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

188 d shear stress specifically up-regulates the epiblast marker Fgf5.

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

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

191 gnificant for priming differentiation during epiblast maturation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 ifferentiation at the expense of maintaining epiblast pluripotency.

208 FGF signaling on exit of the lineage-primed epiblast pluripotent state initiates an early induction

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

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

211 However, epiblast precursors exhibit less plasticity than precurs

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

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

214 mRNA and the cell surface G8 antigen in the epiblast prior to the onset of gastrulation.

215 a stage equivalent to the post-implantation epiblast, prior to germ layer specification and down-reg

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

217 at as AVE movements are being initiated, the epiblast proliferates at a much higher rate than the vis

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

219 ires a certain level of proliferation in the epiblast provides a mechanism whereby A-P axis developme

220 Embryos that lack Rac1 in the epiblast (Rac1Deltaepi) initiate development normally: t

221 Their ablation in the epiblast resulted in eye defects, including anopthalmia,

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

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

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

225 In embryos with an epiblast-specific deletion of Bmpr1a (Bmpr1a(null/flox);

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

227 Epiblast-specific deletion shows that Pten is not requir

228 Epiblast-specific inactivation of Cubn in the mouse embr

229 Erf epiblast-specific knockout embryos had reduced numbers o

230 Throughout the ICM, the epiblast-specific marker Nanog is expressed, and in XX e

231 anization, mimicking mtDNA bottleneck during epiblast specification.

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

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

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

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

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

237 Epiblast-state transition in mESCs involves heparan sulf

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

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

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

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

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

243 Epiblast stem cells (EpiSCs) are pluripotent cells deriv

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

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

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

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

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

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

250 tain pluripotency in human ESCs and in mouse epiblast stem cells (EpiSCs), but the molecular mechanis

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

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

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

254 broblast growth factor to form self-renewing epiblast stem cells (EpiSCs), which exhibit essential pr

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

256 so far corresponds to that of mouse-derived epiblast stem cells (EpiSCs).

257 nic stem (ES) cells and egg cylinder-derived epiblast stem cells (EpiSCs).

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

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

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

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

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

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

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

265 we used human embryonic stem cells and mouse epiblast stem cells to study specification of definitive

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

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

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

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

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

271 in induced pluripotent stem cells and murine epiblast stem cells.

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

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

274 Similarly, in vivo epiblasts suppress COX levels.

275 rk-DOCK180 complex and mediates BM-dependent epiblast survival through activating the phosphatidylino

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

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

278 oes a form of "autosomal Lyonization" in the epiblast that is difficult to reprogram and coincides wi

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

280 We find that in the pluripotent epiblast they inhibit apoptosis by blocking the expressi

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

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

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

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

285 dial component has been fate mapped from the epiblast to the heart in both mammals and birds.

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

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

288 In rodents, the naive early epiblast undergoes profound morphogenetic, transcription

289 The pluripotent mammalian epiblast undergoes unusually fast cell proliferation.

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

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

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

293 By conditionally deleting Tgif1 in the epiblast, we demonstrate that a single wild-type allele

294 ecified in a superficial layer of cells, the epiblast, where cells maintain an epithelioid morphology

295 ion, since Cripto is expressed solely in the epiblast whereas Cryptic is expressed in the primitive e

296 isions are biased toward forming pluripotent epiblast, whereas cells internalized in the next two wav

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

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

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

300 in the mutant EBs rescues the BM-contacting epiblast, while expression of a constitutively active Ra