ライフサイエンスコーパス: dpc

1 26 and 27 somite stages (approximately 10.0 dpc) and became intermingled with pancreatic progenitors

2 At 10.0 dpc, BMP-11 is expressed in the distal and posterior reg

3 Mutant embryos are first recognizable by 7.0 dpc, owing to a characteristic localized outpocketing of

4 At 6.5 dpc, 8.0 dpc and 10.5 dpc, the tetraploid ESCs manifested in the

5 YS and embryonic SP isolated 8.0 dpc expressed vascular endothelial-cadherin (VE-cadherin

6 Fate-mapping the headfold-stage (~7.75-8.0 dpc) posterior region, by which time PGCs are thought to

7 to maintain expression in somite 7 from 9.0 dpc onwards.

8 inus venosa and in the atrium at 8.5 and 9.0 dpc, and in the atria from 10.5 dpc onwards.

9 Mutant embryos died by 10 dpc, probably as a result of placental failure.

10 a sacculi and the cochlea were present at 12 dpc but became distinguishable from each other by 13 dpc

11 ateral crista, and the macula utriculi at 12 dpc.

12 became distinguishable from each other by 13 dpc.

13 When separated 13 dpc rat metanephric mesenchymes were cultured in serum-f

14 Examination of fetuses older than 13 dpc suggests that the presence of ovotestes is transient

15 d tissue in situ hybridization studies of 14-dpc embryos.

16 brain and during mouse embryogenesis (11-17 dpc).

17 -1(+)/CD31(-)/CD34(-)/VE-Cadherin(-)) at 7.2 dpc.

18 roliferation, starting between 9.5 and 10.25 dpc when germ cells begin to migrate to the developing g

19 ressed in posterior heart precursors at 8.25 dpc, in sinus venosa and in the atrium at 8.5 and 9.0 dp

20 mice exhibited mineralization defects by 33 dpc, as expected, but this defect was partially correcte

21 ite 15-17 stages, corresponding to 11.2-11.4 dpc, the coelomic epithelial cells of both sexes migrate

22 ome dependent on FGF9 signaling between 10.5 dpc and 11.5 dpc, and that FGF9 directly promotes XY gon

23 nd that Bmp5;Bmp7 double mutants die at 10.5 dpc and display striking defects primarily affecting the

24 rints, was already initiated in PGCs at 10.5 dpc and was complete by 13.5 dpc.

25 d then undergo erasure at approximately 10.5 dpc as the PGCs enter the genital ridges.

26 Smad1-/- embryos die by 10.5 dpc because they fail to connect to the placenta.

27 8.5 and 9.0 dpc, and in the atria from 10.5 dpc onwards.

28 ession by 9.5 and dynamic expression at 10.5 dpc stages.

29 When PGC nuclei at 8.5, 9.5, and 10.5 dpc were transferred into enucleated oocytes, seven clon

30 this gene from early (8.5 dpc) to late (10.5 dpc) somitogenesis.

31 cts and lethality at mid-gestation (9.0-10.5 dpc).

32 utants does not regress ventrally after 10.5 dpc, as in normal embryos.

33 At 6.5 dpc, 8.0 dpc and 10.5 dpc, the tetraploid ESCs manifested in the same location

34 but appears to be in phase with Lfng by 10.5 dpc.

35 ernal allele-specific methylation until 10.5 dpc.

36 lation was largely erased from Snrpn by 10.5 dpc.

37 cells (PGCs) from earlier stages at 8.5-10.5 dpc.

38 clear transfer, whereas gonadal PGCs at 11.5 dpc and later are incompetent to support full-term devel

39 crista was the first organ to appear at 11.5 dpc and was followed by the superior crista, the lateral

40 genital ridges isolated from embryos at 11.5 dpc are morphologically nonorganized.

41 In contrast, SP isolated 9.5 to 11.5 dpc contained a significantly higher proportion of cells

42 Furthermore, YS SP isolated 9.5 to 11.5 dpc demonstrated 40- to 90-fold enrichment for hematopoi

43 ohistochemical staining of the gonad at 11.5 dpc showed that the basement membrane barrier under the

44 Culturing 11.5 dpc urogenital ridges in the presence of HGF we obtained

45 FGF9 is necessary for 11.5 dpc XY gonocyte survival and is the earliest reported fa

46 phros (AGM) and the fetal liver at 10.5-11.5 dpc, and found that only a rare number of cells displaye

47 on FGF9 signaling between 10.5 dpc and 11.5 dpc, and that FGF9 directly promotes XY gonocyte surviva

48 tly promotes XY gonocyte survival after 11.5 dpc, independently from Sertoli cell differentiation.

49 By 11.5 dpc, the majority of PGCs showed nearly complete or comp

50 inthine layer were observed as early as 11.5 dpc.

51 es until 11.5 days postcoitum (dpc), by 12.5 dpc the XY gonad develops a distinct vasculature.

52 are sequestered inside testis cords by 12.5 dpc where they arrest in mitosis.

53 These mice die at 12.5 dpc with embryos showing severe cardiovascular and facia

54 tail somite 30 stage, corresponding to 12.5 dpc, after testis cords had formed and the basement memb

55 Sertoli cells of embryonic testes from 12.5 dpc, and in granulosa cells of growing follicles in adul

56 As Amhr2-Cre is expressed in gonads at 12.5 dpc, these findings suggest preimplantation selection of

57 ) and total loss of pituitary tissue by 12.5 dpc.

58 entally induced into XX gonads prior to 12.5 dpc.

59 ales, the gonad develops normally until 12.5 dpc.

60 twice that of wild-type littermates at 12.5 dpc.

61 nads from 10.5 days postcoitum (dpc) to 12.5 dpc.

62 ated atlas of the anterior portion of a 13.5 dpc (TS 22) mouse with anatomical structures delineated

63 enta, embryolemma and umbilical cord at 13.5 dpc and 16.5 dpc; however, very less GFP cells were foun

64 ee-dimensional renderings of the entire 13.5 dpc embryo and specific organ systems.

65 Further studies in 8.5 to 13.5 dpc Pin1(-/-) embryos showed that PGCs were allocated pr

66 rm cells spontaneously enter meiosis by 13.5 dpc, and the gonad follows the ovarian fate.

67 In testes isolated from 12.5 and 13.5 dpc, c-met expression is detectable and essentially loca

68 However, by 13.5 dpc, the testis cords are disorganized and incompletely

69 in a markedly reduced number of PGCs at 13.5 dpc.

70 in PGCs at 10.5 dpc and was complete by 13.5 dpc.

71 ssion from 7.5 dpc (days postcoitum) to 14.5 dpc in ectoplacental cone, giant cells, and labyrinthine

72 um (dpc) in developing gut, as early as 14.5 dpc in the cartilage primordium, and in the developing u

73 We also show that when 14.5 dpc XX somatic cells are recombined with XY somatic cell

74 not be induced into normal XX gonads at 14.5 dpc, it can be induced into XX gonads depleted of germ c

75 By 14.5 dpc, these gonads contain germ cells that enter meiosis

76 At 14.5 dpc, we found evidence for premature neural precursor ce

77 demonstrates expression of IIb mRNA by 14.5 dpc, which proceeds developmentally in a rostral to caud

78 diac development began between 11.5 and 14.5 dpc.

79 st detected in the mouse metanephros at 14.5 dpc; transcript abundance increased with gestational age

80 nduction velocity was seen in the RV at 15.5 dpc (in cm/second, mean [1 SE confidence interval], WT 9

81 n, and the embryos die between 10.5 and 15.5 dpc due to cardiac insufficiency.

82 By 15.5 dpc, very intense beta-gal staining localizes to the duc

83 n be detected in the ductus as early as 15.5 dpc.

84 In 14.5-16.5 dpc (days post-conception) mouse embryos, Esrrg localize

85 beta1-integrin null lenses are seen at 16.5 dpc when the epithelium becomes disorganized and begins

86 Speg mutant hearts began to enlarge by 16.5 dpc, and by 18.5 dpc, they demonstrated dilation of righ

87 l cells surrounding the oocyte cysts on 16.5 dpc, and in stromal cells surrounding growing follicles

88 At 16.5 dpc, male embryos lacking both genes exhibit multiple de

89 At 16.5 dpc, the reduction in lung volume was due to loss of lun

90 Beginning around 16.5 dpc, when Shh and Ptc RNA levels are normally both decli

91 emma and umbilical cord at 13.5 dpc and 16.5 dpc; however, very less GFP cells were found in the fetu

92 .7; P<0.005]) and in both ventricles at 17.5 dpc (in RV, WT 8.4 [7.6 to 9.3], Cx43(+/)(-) 8.7 [8.1 to

93 able in ventricular homogenates even at 17.5 dpc, probably accounting for the residual conduction fun

94 the pulmonary trunk and aortic arch; by 17.5 dpc, the smooth muscle layers of the tunica media in the

95 ithelial cell proliferation at 16.5 and 17.5 dpc.

96 al hernia were also observed in ablated 18.5 dpc embryos.

97 In contrast, at late fetal stages (18.5 dpc), cells that were Shh-responsive but postmitotic wer

98 At 18.5 dpc, limb skeletons of Ihh, PTHrP compound mutants were

99 At 18.5 dpc, the hearts were significantly smaller, with reduced

100 ts began to enlarge by 16.5 dpc, and by 18.5 dpc, they demonstrated dilation of right and left atria

101 n becomes localized to renal papilla by 18.5 dpc.

102 mooth muscle cells, did not begin until 18.5 dpc.

103 dergo programmed breakdown between 20.5-22.5 dpc, during which approximately 33% of the oocytes survi

104 and trophectoderm, and implant (roughly 4.5 dpc), indicating that CUL-4A(-/-) embryos die between 4.

105 At 3.5 days post-coitum (dpc) and 4.5 dpc, the tetraploid ESCs were able to contribute to the

106 AVE is induced at the distal tip of the 5.5 dpc embryo and then migrates to the prospective anterior

107 st in the posterior visceral endoderm of 5.5 dpc embryos and later in the posterior epiblast.

108 derm of the implanting blastocyst but by 5.5 dpc its transcripts are present only in a small patch of

109 i-implantation lethality between 3.5 and 5.5 dpc.

110 os by deletion of bax allows survival to 6.5 dpc and alters the mechanism of death from apoptosis to

111 one-fourth of all implantation sites at 6.5 dpc appeared empty with no intact embryos present.

112 At 6.5 dpc, 8.0 dpc and 10.5 dpc, the tetraploid ESCs manifeste

113 In embryos dissected between 5.5 and 6.5 dpc, Brachyury is first expressed in the distal extra-em

114 ly expressed in the visceral endoderm at 6.5 dpc, in other tissues Smad1 is co-expressed with Smad5 a

115 bryogenesis detect Plac1 expression from 7.5 dpc (days postcoitum) to 14.5 dpc in ectoplacental cone,

116 Marked expansion of nodal expression in 7.5 dpc embryos and variable degrees of node dysmorphology i

117 By 7.5 dpc, Smad1-deficient embryos show a marked impairment in

118 at neural plate/headfold stages (NP/HF, ~7.5 dpc-8 dpc) represents an optimal window from which heman

119 ue to p53-initiated cell cycle arrest at 7.5 dpc.

120 CUL-4A(-/-) embryos die between 4.5 and 7.5 dpc.

121 embryonic ectoderm of mutant embryos at 7.5 dpc.

122 pc), but development was arrested before 7.5 dpc.

123 opment, with embryos dying approximately 7.5 dpc.

124 g null embryos, Nrarp appeared static at 8.5 dpc but resumed cycling expression by 9.5 and dynamic ex

125 ling expression of this gene from early (8.5 dpc) to late (10.5 dpc) somitogenesis.

126 Mdm4-null mice died at 7.5-8.5 dpc, owing to loss of cell proliferation and not inducti

127 uired to maintain this expression beyond 8.5 dpc.

128 .5 days postcoitum (dpc) and resorbed by 8.5 dpc.

129 o Lfng and Axin2 (a Wnt pathway gene) at 9.5 dpc but appears to be in phase with Lfng by 10.5 dpc.

130 Thus, migrating PGCs at 8.5-9.5 dpc can be successfully used as donors for nuclear trans

131 istent with this possibility, embryos at 9.5 dpc had significantly elevated levels of retinoic acid a

132 bryogenesis, BMP-11 is first detected at 9.5 dpc in the tail bud with expression becoming stronger as

133 as evident on the H19 paternal allele at 9.5 dpc, most PGCs did not demonstrate significant erasure o

134 is arrested at the thyroid bud stage at 9.5 dpc.

135 dpc), and excessive cell death occurs at 9.5 dpc.

136 pc), and all the null embryos die before 9.5 dpc.

137 genitor cells of the somite beginning at 9.5 dpc.

138 tiation in the atrioventricular canal at 9.5 dpc.

139 to pregnant mice at 7.5, but not after 8.5, dpc induced cardiac dismorphology, ranging from complete

140 ver, this sexual bias is not obvious in 10.5-dpc embryos, a developmental stage before the sexual dif

141 he remaining two offspring derived from 10.5-dpc PGCs, one died shortly after birth, and the other sh

142 imprinted H19 and Snrpn loci in 9.5- to 11.5-dpc PGCs.

143 mouse embryonic fibroblasts (MEFs) from 12.5-dpc embryos, which revealed that NRC(-/-) MEFs exhibit a

144 ost obvious in the developing brains of 14.5-dpc embryos, but also detected in the brains of postnata

145 Similarly, clones derived from male 15.5-dpc germ cells showed increased methylation correlating

146 However, histological examination of 6.5-dpc implantation sites revealed the presence of embryo r

147 Nlvcf is expressed in most structures of 9.5-dpc mouse embryos, with especially high expression in th

148 mprints remain largely intact in 8.5- to 9.5-dpc PGCs and then undergo erasure at approximately 10.5

149 Of these, five, all derived from 8.5- or 9.5-dpc PGCs, developed into healthy adults with normal fert

150 These data suggest that 9.5-dpc yolk sac- and P-Sp-derived primary Tie2-GFP+Flk-1+CD

151 ite 18-20 stages, corresponding to 11.5-11.7 dpc, the coelomic epithelial cells no longer became Sert

152 -PCR and on Northern blots of tissues from 7-dpc embryos.

153 riable degrees of node dysmorphology in 7.75 dpc embryos suggested that the pathogenesis of the cardi

154 y in somitogenesis, which terminates by 8.75 dpc.

155 ceding the formation of blood vessels (7.5-8 dpc) in the embryo proper, yolk sac, and allantois, the

156 ral plate/headfold stages (NP/HF, ~7.5 dpc-8 dpc) represents an optimal window from which hemangiobla

157 ut this defect was partially corrected by 96 dpc.

158 , and that AID(GFP+) cells are detectable at dpc 11.5 and 12.5.

159 Fetal rat metatarsal bones (dpc 20) were cultured in serum-free medium for 7 days in

160 on in RP epithelium at 9.0 days post coitum (dpc) and total loss of pituitary tissue by 12.5 dpc.

161 d-type embryos through 6.5 days post coitum (dpc) and were able to establish all three germ layers.

162 erm line originates at 6.5 days post coitum (dpc) in the proximal epiblast, apparently in response to

163 derived from 11.5 or 12.5 days post coitum (dpc) primordial germ cells (PGCs).

164 duced and patterned at 7.5 days post coitum (dpc), but subsequently fails to develop.

165 nd yolk sac defects at 9.5 days post coitum (dpc), including disrupted angiogenesis in mesoderm deriv

166 Gm114 begins at 12.5-13.5 days post coitum (dpc), the stage in mice when germ cells cease proliferat

167 size with controls at 13.5 days post coitum (dpc), their placentas were significantly larger.

168 line in numbers after 11.5 days post coitum (dpc), while germ cell numbers in XX gonads are unaffecte

169 he gonads from 8.5 to 13.5 days post coitum (dpc).

170 kedly between 9.5 and 12.5 days post coitum (dpc).

171 t XX gonads from 11.5-16.5 days post coitum (dpc).

172 died between 8.5 and 10.5 days post coitum (dpc).

173 heart starting at day 11.5 days post coitum (dpc).

174 and ovary as early as 13.5 days post coitum (dpc).

175 on 12.5, 14.5, 16.5, and 18.5 d post coitum (dpc).

176 At 3.5 days post-coitum (dpc) and 4.5 dpc, the tetraploid ESCs were able to contr

177 NOS) expression in 7.2-8.5 days post-coitum (dpc) mouse embryos.

178 air (-s) stages (~6.75-9.0 days post coitum, dpc) in histological sections.

179 ndothelial cells from 9.5-days after coitus (dpc) yolk sac and P-Sp.

180 yonic tissues 7.5 to 11.5 days after coitus (dpc), resolved an SP in each, and demonstrated that thes

181 stage at approximately 6.5 days post coitus (dpc), but development was arrested before 7.5 dpc.

182 ber differentiation at 9.5 days post coitus (dpc).

183 cells starting at 10.5 days post conception (dpc), and that AID(GFP+) cells are detectable at dpc 11.

184 n in Cx43(-/-) ventricles at postcoital day (dpc) 12.5 compared with WT or Cx43(+/)(-) ventricles.

185 ified as the candidate tumor suppressor gene dpc-4, reconstitutes TGF-beta- and activin-dependent tra

186 velopmental stages 23 to 96 days postcoital (dpc) were examined by light microscopy.

187 ears ranging from 10.25 to 17 d postcoitum (dpc) were filled with paint to reveal their gross develo

188 mouse embryos commencing at 10 d postcoitum (dpc), beyond the period of primary dorsal-ventral patter

189 firmed by genotyping of 12.5-day-postcoitum (dpc) embryos.

190 embryos arrested after 5.5 days postcoitum (dpc) and resorbed by 8.5 dpc.

191 was followed for up to 18.5 days postcoitum (dpc) and that approximately 90% of GYS1-null animals die

192 dal germ cells at 11.5-19.5 days postcoitum (dpc) are incompetent to support full-term development of

193 ybridization as early as 10 days postcoitum (dpc) in developing gut, as early as 14.5 dpc in the cart

194 immunofluorescence at 13.5 days postcoitum (dpc) in the mesenchyme surrounding the ductus.

195 to form shortly before 10.5 days postcoitum (dpc) on the ventromedial side of the mesonephros.

196 developing gonads from 10.5 days postcoitum (dpc) to 12.5 dpc.

197 ant embryos as early as 7.5 days postcoitum (dpc) were recovered.

198 is retarded globally by 7.5 days postcoitum (dpc), and all the null embryos die before 9.5 dpc.

199 mental process stops at 8.5 days postcoitum (dpc), and excessive cell death occurs at 9.5 dpc.

200 Y genital ridges until 11.5 days postcoitum (dpc), by 12.5 dpc the XY gonad develops a distinct vascu

201 At E12.5 days postcoitum (dpc), FVII(-/-)/PC(-/-) embryos demonstrated an intra- a

202 cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure.

203 apoptosis initiated at 3.5 days postcoitum (dpc).

204 absent between 6.5 and 12.5 days postcoitum (dpc).

205 olated from embryos at 11.5 days postcoitum (dpc).

206 urulation and die before 11 days postcoitum (dpc).

207 /v positions at 9.5 to 12.5 days postcoitum (dpc).

208 bryos died in utero by 18.5 days postcoitum (dpc).

209 G9a null embryos die at 8.5 days postcoitum (dpc).

210 cloned from migrating 10.5-days-postcoitum (dpc) primordial germ cells (PGCs) showed normal morpholo

211 estation (approximately 9.5 days postcoitum [dpc]) and exhibited a number of novel phenotypes, includ

212 antoises (approximately 8.0 days postcoitum; dpc) were subdivided into three proximodistal regions an

213 os die between 8.5 and 12.5 days postcoitus (dpc), suggesting that NRC has a pleotrophic effect on gr

214 PCR reactions using a 15-day-postconception (dpc) whole-mouse embryo cDNA library.

215 fixed embryos 6 to 15.5 days postconception (dpc) [Theiler Stages (TS) 8 to 24]; (2) an annotated atl