ライフサイエンスコーパス: mutant embryo

1 e severe than that observed in either single-mutant embryo.

2 in transcription factors, was reduced in the mutant embryo.

3 y defects, and abnormal contractions in POMT mutant embryos.

4 transcripts are dramatically reduced in lis1 mutant embryos.

5 an unfused nasal capsule and palatine in the mutant embryos.

6 istry similar to that characterized in Dact1 mutant embryos.

7 artially suppressed the EMT defect in Bmp4/7 mutant embryos.

8 ema3E morphant embryos, as well as in sema3D mutant embryos.

9 ased apoptosis in neural crest structures in mutant embryos.

10 clopamine prevented colobomas in ptch2(uta1) mutant embryos.

11 xpression, and this is undetectable in Hoxa2 mutant embryos.

12 members of the Wnt pathway in wild-type and mutant embryos.

13 l neurons) is suppressed in comm, cno double-mutant embryos.

14 the gut endoderm in wild-type but not Sox17 mutant embryos.

15 ve axons aberrantly cross the midline in cno mutant embryos.

16 npt2a, are significantly affected in entpd5 mutant embryos.

17 incisor epithelium of both Ikkalpha and Irf6 mutant embryos.

18 MEOBOX5 were found in heart-stage bps triple-mutant embryos.

19 oping at Snail target genes in wild-type and mutant embryos.

20 K27me3, and H3K4me3 in extra sex combs (esc) mutant embryos.

21 velopment is defective in both ise1 and ise2 mutant embryos.

22 e detected shift in glycan complexity in sff mutant embryos.

23 ed as early as E12.5 in SM22Cre(+)Ilk(Fl/Fl) mutant embryos.

24 d ECM proteins are properly localized in msk mutant embryos.

25 ated by the partially penetrant lethality of mutant embryos.

26 on of the thoracic aorta was observed in ILK mutant embryos.

27 ted protein kinase (MAPK) are reduced in msk mutant embryos.

28 ent or greatly reduced in Etsrp knockdown or mutant embryos.

29 genes were significantly up-regulated in the mutant embryos.

30 t activated by Bcd, becomes more variable in mutant embryos.

31 re not LAFL targets were derepressed in val1 mutant embryos.

32 MPs purified from wild-type (WT) or mindbomb mutant embryos.

33 and is mislocalized in both cct and in dfmr1 mutant embryos.

34 proper BMP signaling output in wild-type and mutant embryos.

35 otide synthesis and energy production in the mutant embryos.

36 n the forebrain and dorsal root ganglions of mutant embryos.

37 tify proteins that are misexpressed in dfmr1 mutant embryos.

38 Nrk2b-deficient embryos, but not in laminin mutant embryos.

39 d expression of fibronectin 1 (fn1) in hand2 mutant embryos.

40 al granules in insulin-expressing cells from mutant embryos.

41 tion in wild-type and sox9 single and double mutant embryos.

42 d remarkably normal in homozygous Hand2(EDE) mutant embryos.

43 ng to the caudal dysgenesis phenotype of acd mutant embryos.

44 after crossing, reminiscent of Neuropilin-2 mutant embryos.

45 in vivo, we examined motor axon guidance in mutant embryos.

46 uction of dia enhances actin defects in Apc2 mutant embryos.

47 hypertrophy of sympathoadrenal cells in nf1 mutant embryos.

48 nces in cell-shape dynamics in wild-type and mutant embryos.

49 ptomics of wild-type and Fgf receptor (Fgfr) mutant embryos.

50 Osr1(+/-), Osr1(-/-) and Tbx5(+/-)/Osr1(+/-) mutant embryos.

51 ained an altered expression pattern in Abph2 mutant embryos.

52 genic reporter substrate in wild-type and PC mutant embryos.

53 expanded the domain of thoracic identity in mutant embryos.

54 iminated the residual denticles found in svb mutant embryos.

55 ansport (IFT) protein-encoding loci in Atmin mutant embryos.

56 he auxin efflux carrier were affected in vcc mutant embryos.

57 ignalling appears to underlie exencephaly in mutant embryos.

58 antly lower frequencies in control or single-mutant embryos.

59 in the developing palatal mesenchyme in Pax9 mutant embryos.

60 eural plate in wild-type embryos, but not in mutant embryos.

61 ity at E14.5 with severe liver hemorrhage in mutant embryos.

62 se changes are not seen in heterozygous Tbx1 mutant embryos-a 22q11 gene thought to explain much of 2

63 CERT mutant embryos accumulate ceramide in the ER but also mi

64 Mutant embryos additionally feature reduced vSMC coverag

65 talpid(3) mutant embryos also develop polycystic kidneys, consiste

66 Interestingly, brom bones mutant embryos also display defects in dorsoventral axis

67 Wnt1 mutant embryos also have alterations in a hierarchical g

68 These mutant embryos also lacked the early defects in growth o

69 of clock desynchronisation in Notch pathway mutant embryos and also that Notch-mediated synchronisat

70 Interestingly, Traf3ip1 mutant embryos and cells failed to show alterations in I

71 d the BMP activity gradient in wild-type and mutant embryos and combined these data with a mathematic

72 x interplay between them, we analyzed double mutant embryos and compared their phenotypes to the sing

73 show that in mef2ca(b1086) loss of function mutant embryos and early larvae, development of craniofa

74 e lineage is increased in pax7a/pax7b double-mutant embryos and larvae, whereas juvenile and adult pa

75 tion of CDC-48.3 restores viability to air-2 mutant embryos and leads to abnormally high AIR-2 levels

76 Here we show that homozygous Abl mutant embryos and newborns on the C57BL/6J background,

77 itors among transcripts downregulated in the mutant embryos and several extracellular matrix proteins

78 s not properly localize at the furrow in nuf mutant embryos and that RhoGEF2-Rho1 pathway components

79 scleraxis-expressing TNPs is not affected in mutant embryos and the tendon phenotype is first manifes

80 By analyzing mutant embryos and through targeted genetic perturbation

81 f8 and Wnt3a, is down regulated in Brachyury mutant embryos and we demonstrate that they are also Bra

82 is impaired in Wnt5a(-/-)Wnt5b(-/-) and Sfrp mutant embryos, and also in the presence of a uniform di

83 e defects are observed in Gnai3/Gnai1 double-mutant embryos, and crosses with a conditional allele of

84 tion and neural tube patterning in talpid(3) mutant embryos, and is sufficient for centrosomal locali

85 le those observed in Sema-1a- and PlexA-null mutant embryos, and perlecan mutants genetically interac

86 veloping minor SGs are absent in Eda pathway mutant embryos, and these mice exhibit a dysplastic circ

87 of genes regulating tendonogenesis in dd/dd mutant embryos, and we determined that retinoic acid (RA

88 In wild-type and Ncd null mutant embryos, anti-KLP61F dissociated the motor from s

89 ighly conserved RNA-binding protein and hoip mutant embryos are largely paralytic due to defects in m

90 Er71 mutant embryos are nonviable and lack hematopoietic and

91 rylation levels, between wild-type and pig-1 mutant embryos are predominantly connected with processe

92 cdc-42 mutant embryos arrest during elongation with epidermal r

93 Although cell polarity appeared normal, Klf5 mutant embryos arrested at the blastocyst stage and fail

94 Developmental arrest of Blimp1/Prdm1 mutant embryos at around embryonic day 10.5 (E10.5) has

95 c cultures of skin explants from control and mutant embryos at embryonic day 15.5.

96 velopment and the death of homozygous Fbxl10-mutant embryos at midgestation.

97 f this pathway are affected in Gbx2 and Tbx1 mutant embryos at the time of PAA development.

98 l metabolism is compromised severely in ise1 mutant embryos, because their mitochondrial proton gradi

99 w that excess Hbs rescues some fusion in sns mutant embryos beyond precursor formation, consistent wi

100 (um18) could not rescue lymphatic defects in mutant embryos, but induced ectopic blood vessel branchi

101 endothelial tearing, leading to lethality of mutant embryos by E9-10 due to failed blood circulation.

102 Consistent with this, entpd5 mutant embryos can be rescued by high levels of inorgani

103 ng that the extra-embryonic tissues in these mutant embryos can sustain development to organogenesis

104 Homozygous mutant embryos carry a C->A transversion, that changes a

105 Like null mutants, embryos carrying a targeted deletion of exon 7

106 onversely, nuclei in both Kinesin and Dynein mutant embryos change direction more often and do not ma

107 floor plate cilia are disorganized in vangl2 mutant embryos, cilia appear to be dispensable for neuro

108 Jabba mutant embryos compensate for this histone deficit by tr

109 Mutant embryos contain normal numbers of E10.5 intraaort

110 f cardiac progenitors in RBPJ and RBPJ/Axin2 mutants, embryo cultures in the presence of the Bmp inhi

111 ious studies have shown that spadetail (spt) mutant embryos, defective in tbx16 gene function, fail t

112 a(cko/cko), and Klf1(wt/ko)::Bcl11a(cko/cko) mutant embryos demonstrated increased expression of mous

113 ide levels rescued epithelial defects in crb mutant embryos, demonstrating that limitation of superox

114 eath is rescued in Sas4(-/-) p53(-/-) double-mutant embryos, demonstrating that mammalian centrioles

115 However, homozygous mutant embryos develop normally and adults are healthy a

116 Mutant embryos develop partially penetrant NTDs while su

117 We report that sec13(sq198) mutant embryos develop small eyes that exhibit disrupted

118 defects in vein connectivity appear early in mutant embryo development.

119 Mutant embryos did not develop an effective barrier to t

120 ion of the brains of E18.5 Nmnat2(blad/blad) mutant embryos did not reveal any obvious morphological

121 The resulting Slb mutant embryos die between E12.5 and 13.0, and exhibit s

122 Chd4 mutant embryos died before birth and exhibited severe ed

123 We report that nearly all PIKfyve(KO/KO) mutant embryos died before the 32-64-cell stage.

124 grating into the developing liver, and Gata4-mutant embryos died from subsequent liver hypoplasia and

125 Using Rdh10(trex)-mutant embryos, dietary supplementation of retinaldehyde

126 Mutant embryos display a loss of birefringency in their

127 xnd-1 mutant embryos display a novel 'one PGC' phenotype as a

128 oral epithelia, and mouse Irf6 targeted null mutant embryos display abnormal differentiation of oral

129 Mutant embryos display accumulation of mesenchymal cells

130 Mutant embryos display increased levels of acetylated p5

131 Dkk1-null mutant embryos display severe defects in head induction.

132 In addition, nau mutant embryos display thinner muscle fibres.

133 7 hour post fertilization (hpf) MZ ewsa(m/m) mutant embryos displayed a higher incidence of aberrant

134 Piriform cortex neurons from E14.5 mutant embryos displayed axon initiation/outgrowth delay

135 Fancd2/Mlh1 double-mutant embryos displayed growth retardation resulting in

136 with a functional disruption of Nups, ooc-5-mutant embryos displayed impaired nuclear import kinetic

137 Surprisingly, we found that mutant embryos displayed numerous defects related to the

138 Further examination revealed that mutant embryos displayed severe molecular defects starti

139 al mutant alleles to generate Rb;p107 double-mutant embryos (DKOs) that develop in the absence of pla

140 In Tgfbr2 mutant embryos, downregulation of Ctgf expression is ass

141 h of the palate was severely impaired in the mutant embryos, due to decreased cell proliferation.

142 Although Pofut2 mutant embryos established anterior/posterior polarity,

143 Myotubes fail to elongate in hoip mutant embryos, even though the known regulators of soma

144 Surprisingly, mutant embryos eventually correct the myocardial deficit

145 Mutant embryos eventually recover and undergo relatively

146 These mutant embryos exhibit a defect in the clearance of apop

147 tachment sites in late embryogenesis and msk mutant embryos exhibit a failure in muscle-tendon cell a

148 Homozygous Ddx18 mutant embryos exhibit a profound loss of myeloid and er

149 teract in this lineage, as double-homozygous mutant embryos exhibit an overt facial clefting phenotyp

150 zebrafish embryo; consistent with this, fro mutant embryos exhibit defects specifically in their fas

151 These mutant embryos exhibit fragmented or decondensed nuclei

152 Here we show that Crkl mutant embryos exhibit gene dosage-dependent growth rest

153 f elevation in wild-type littermates, Golgb1 mutant embryos exhibit increased cell density, reduced h

154 S-2 also promotes differentiation, and mes-2 mutant embryos exhibit prolonged developmental plasticit

155 Nisch-mutant embryos exhibited delayed development, characteri

156 Furthermore, lines mutant embryos exhibited gonads containing excess hub ce

157 However, Hand2(EDE) mutant embryos exhibited growth defects in the limb buds

158 While a fraction of double-mutant embryos exhibited midgestation abnormalities with

159 Line2F homozygous mutant embryos fail to close the neural tube, body wall,

160 network can have indeterminate effects: some mutant embryos fail to develop intestinal cells, whereas

161 The double mutant embryos fail to initiate root and shoot meristems

162 phogenesis, the Osr2(-/-)Runx2(-/-) compound mutant embryos failed to activate the expression of Fgf3

163 Mutant embryos failed to establish normal auxin gradient

164 notype of this nucleus in single or compound mutant embryos for the Onecut factors.

165 Weak double mutant embryos give rise to viable seedlings with dramat

166 In Rpl38 mutant embryos, global protein synthesis is unchanged; h

167 ha mutants developed normally; however, shha mutant embryos globally expressing Cre exhibited strong

168 in zebrafish foxd3(zdf10);tfap2a(low) double mutant embryos globally prevents the specification of de

169 cle promotes left-right asymmetry and iguana mutant embryos had left-right asymmetry defects.

170 Unlike Brg1 mutants, Chd4 mutant embryos had normal yolk sac vascular morphology.

171 Mutant embryos had reduced chondrocyte proliferation and

172 Dicer mutant embryos had reduced expression of Dlx2, a transcr

173 The developing heart of null mutant embryos has smaller chambers and reduced myocardi

174 Mutant embryos have a decrease in the number of prolifer

175 se, embryonic fibroblast cells cultured from mutant embryos have a severe proliferation defect, as we

176 Additionally, Chd7 mutant embryos have CHD7 dosage-dependent reductions in

177 abl mutant embryos have decreased beta-catenin turnover at s

178 Rsg1 mutant embryos have fewer primary cilia than wild-type e

179 Med31 mutant embryos have fewer proliferating cells than contr

180 lture assays, we demonstrate that the Golgb1 mutant embryos have intrinsic defects in palatal shelf e

181 In Jabba mutant embryos, histones H2a and H2b are degraded but em

182 the heart in fibronectin- or integrin alpha5-mutant embryos, however, the hearts in these mutants are

183 erm cell migration appeared normal within Ft mutant embryos; however, germ cell counts progressively

184 h this, XEN cells could be derived from Fgf4 mutant embryos in which PrE had been restored and these

185 s of T cell development in Gata3 hypomorphic mutant embryos, in irradiated mice reconstituted with Ga

186 In ptc1(-/-) and ptc2(-/-) mutant embryos, in which Hh signalling is maximal throug

187 in Sfrp1 and Sfrp2 single and compound mouse mutant embryos, in which RGC axons make subtle but signi

188 ng is elevated in the rostral portion of the mutant embryo, including in a domain in or near the zona

189 cy is observed for thousands of genes in esc mutant embryos, including genes not directly regulated b

190 of triangular-shaped muscles observed in col mutant embryos indicate that transient binding of elonga

191 palatal epithelium in the Bmpr1a conditional mutant embryos, indicating that Bmp signaling regulates

192 rmp protein and lrmp RNA is defective in fue mutant embryos, indicating that correct targeting of lrm

193 e ventralized neural tube phenotypes of Sufu mutant embryos, indicating that the Gli3 repressor can f

194 a severely dilated ER in the fetal liver of mutant embryos, indicative of alteration in ER homeostas

195 Thus, Fgf4 mutant embryos initiated the PrE program but exhibited d

196 the etiology of anemia in conditional Gata2 mutant embryos involved HSC loss in the fetal liver, as

197 hesions in the most severely affected double mutant embryos ( Irf6(+/-);Tg(KRT14::Spry4)).

198 spinal closure in pre-spina bifida Zic2(Ku) mutant embryos is associated with altered tissue biomech

199 hat the defect in Hb boundary positioning in mutant embryos is directly reflective of an altered Bcd

200 egarding their gene expression in normal and mutant embryos is one of the significant advantages that

201 Nodal levels in aplnra/b morphant and double mutant embryos is sufficient to rescue cardiac different

202 Although the phenotype of the mutant embryos is variable, the majority have a complete

203 In both Bmp and miRNA-17-92 mutant embryos, Isl1 and Tbx1 expression failed to be co

204 size of the ICM was unaffected in Fgf4 null mutant embryos, it entirely lacked a PrE layer and exclu

205 Here, we show that cells of talpid(3) mutant embryos lack primary cilia and that primary cilia

206 e disruption strategy, we found that Etsrp71 mutant embryos lacked endocardial/endothelial lineages a

207 on profiling to compare wild-type embryos to mutant embryos lacking activity for both sox9a and sox9b

208 ortex and analysis of expression patterns in mutant embryos lacking cD2 or Tbr2 indicate that cD2 is

209 xia-induced prophase arrest is suppressed in mutant embryos lacking nucleoporin NPP-16/NUP50 function

210 HLH54F mutant embryos, larvae, and adults lack all longitudinal

211 thin the plane of the tissue, whereas Vangl2 mutant embryos maintain tissue polarity and basal protru

212 in mice results in embryonic lethality, with mutant embryos manifesting prominent defects in the hear

213 uggest that abnormal Shh signaling in Arl13b mutant embryos may result from defects in protein locali

214 In Dcc mutant embryos, mispositioning of SGNs occurred along th

215 re activated normally in sonic hedgehog(-/-) mutant embryos, Myf5 expression in newly forming somites

216 In Bmp mutant embryos, myocardial differentiation was delayed,

217 ptal defects in approximately half of double-mutant embryos or neonates; miR-133a double-mutant mice

218 itions to compare their outcome with that of mutant embryos or of embryos submitted to exogenous trea

219 ta signaling in Tgfb2(-/-);Tgfb3(-/-) double mutant embryos or through inactivation of the type II TG

220 ar ( approximately 32-cell) stage, dcl1-null mutant embryos overexpress approximately 50 miRNA target

221 MO injection into either wild-type or p53-/- mutant embryos phenocopies cey, indicating that loss of

222 In addition, E(spl)-C mutant embryos phenocopy the cardiac defects of Stat92E

223 hedgehog (Hh) signaling rescued ASDs in Tbx5 mutant embryos, placing Tbx5 upstream or parallel to Hh

224 In addition, l(1)sc mutant embryos possess defects in the formation of MP4-6

225 In disc1 mutant embryos, proliferating rx3+ hypothalamic progenit

226 yer origins suggested that defects in Pofut2 mutant embryos resulted from abnormalities in the extrac

227 ling of Ednrb-iCre expressing cells in Foxd3 mutant embryos revealed a reduction of ENPs throughout t

228 Analysis of Neurexin IV and wrapper mutant embryos revealed identical defects in glial migra

229 Time-lapse SPIM imaging of wild-type and mutant embryos revealed significant and dynamic gaps bet

230 ultivated mouse embryos and of Emx2 and Gli3 mutant embryos revealed that ectopic Fgf8 signalling pro

231 In the mouse, analysis of Sprouty mutant embryos revealed that increased ERK signaling sup

232 tion of these and other TFs in wild type and mutant embryos, revealed a cascade of regulation integra

233 Clone formation in mutant embryos reveals that the transcription factor Ath

234 The data suggest that the morphology of mutant embryo sacs influences endosperm development, lea

235 Here, we show that in glc mutant embryo sacs one sperm cell successfully fuses wit

236 Cells in mutant embryos show abnormal dilation of the ER and dege

237 he situation in mp mutants, obe1 obe2 double mutant embryos show auxin maxima at the root pole and in

238 Mutant embryos show Raldh2 downregulation in the lateral

239 The vcc ops double mutant embryos showed a complete loss of high-complexity

240 Mutant embryos showed delayed palate elevation, stage-sp

241 Double homozygous chmp1a chmp1b mutant embryos showed limited polar differentiation and

242 In addition, some mutant embryos showed poor formation and abnormal alloca

243 Importantly, mutant embryos showed significantly enlarged endocardial

244 RNA-seq on PEAT mutant embryos showed that loss of PEAT modestly increas

245 of hindbrain post-crossing axons in Robo1/2 mutant embryos showed that Slit-Robo repulsive signaling

246 Atm/Hus1 double-mutant embryos showed widespread apoptosis and died mid-

247 Analysis of silent heart mutant embryos shows that initial lumen formation in the

248 Activation of rac1 in mew mutant embryos significantly rescued the gland migration

249 of morphant phenotypes were not observed in mutant embryos, similar to our mutant collection.

250 In Nedd4 mutant embryos, skeletal muscle fiber sizes and motoneur

251 In Foxc1/2 double-mutant embryos, somitogenesis is severely affected, prec

252 Here we report that in Spry1, Spry2 compound mutant embryos (Spry1(-)/(-); Spry2(-)/(-) embryos), the

253 alyses of ENS-lineage and differentiation in mutant embryos suggested activation of a compensatory po

254 pressing cells within the interior of Pofut2 mutant embryos suggested that POFUT2 activity was also r

255 6a/Swap70b morphants resemble Ppt/Slb double mutant embryos suggesting that Swap70b and Def6a delinea

256 levels persisted in maternal-zygotic dicer1 mutant embryos, suggesting that microRNAs contribute to

257 athway, is present at normal levels in spn-2 mutant embryos, suggesting that the degradation pathway

258 hat are not detected in Ret, Gata3 or Raldh2 mutant embryos, suggesting that these protrusions may no

259 nt were upregulated in unaffected Twsg1(-/-) mutant embryos, suggesting that they may compensate for

260 e I nucleoplasmic reticulum in triple seipin mutant embryos, supporting that SEIPINs are essential fo

261 slow postgerminative growth are seen only in mutant embryos that develop on maternal plants with muta

262 Mutant embryos that develop on plants with wild-type sta

263 nstriction produces similar flow patterns in mutant embryos that fail to form cells before gastrulati

264 the late primitive streak of all Axin2(canp) mutant embryos that is associated with the formation of

265 f HPL-2 in vivo appears relatively normal in mutant embryos that lack H3K9me, demonstrating that the

266 transition to a columnar epithelium fails in mutant embryos that lack the tumor suppressor PTEN, alth

267 bed and analyzed a similar phenotype in POMT mutant embryos that shows left-handed body torsion.

268 Consistently, many mutant embryos that survived to embryonic day 8.5 displa

269 We found that in Intu mutant embryos the expression of Gli1 and Ptch1, two dir

270 This function is direct because in Mdr49 mutant embryos the Hh ligand is inappropriately sequeste

271 esp2 mutant, in the zebrafish Mesp quadruple mutant embryos the positions of somite boundaries were c

272 In Onecut mutant embryos, the A13 neurons differentiate normally b

273 subdivided into four phases and, in Stat92E mutant embryos, the broad phase 2 expression pattern in

274 e heart tube is not affected in leo1(LA1186) mutant embryos, the differentiation of cardiomyocytes at

275 In Brn3a mutant embryos, the fasciculus retroflexus is directed a

276 he expression of Notch pathway genes in FgfR mutant embryos, these findings indicate that Notch lies

277 r show that in UTX H3K27 histone demethylase mutant embryos, these genes are even more slowly reactiv

278 The ability of Pofut2 mutant embryos to form teratomas comprised of tissues fr

279 alyzed transcription profiles of control and mutant embryos to identify genes that are regulated by H

280 In addition, we found that Nle1 mutant embryos undergo caspase-mediated apoptosis as hat

281 Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system

282 pendent criteria, to observe a defect in the mutant embryos until the early tailbud stage.

283 in newly forming somites is delayed in Zic2 mutant embryos until the time of Zic1 activation, and bo

284 Somite number remains normal in mutant embryos up until the death of the embryos more th

285 Mutant embryos up-regulated stress responses at sites of

286 In LMO4;SCL compound mutant embryos, V2a-interneurons increase markedly at th

287 Loss of mutant embryos was associated with both defects in place

288 The absence of phenotypes in mutant embryos was not likely due to maternal effects or

289 Ventricular cardiomyocyte proliferation in mutant embryos was restored to normal at E14.5, concurre

290 However, no str1(-/-)/str2(-/-) double mutant embryos were able to develop past the heart stage

291 he edema and hemorrhage in conditional Gata2 mutant embryos were due to defective lymphatic developme

292 the corresponding cells in the node of Acvr1 mutant embryos were proliferative and showed a dramatic

293 g of ISE1 and ISE2 phenocopies ise1 and ise2 mutant embryos: when wild-type ISE1 and ISE2 functions a

294 thick veins mutant embryos, which exhibited defects in the actin cab

295 ymmetry signal by analyzing mouse Sox17 null mutant embryos, which possess endoderm-specific defects.

296 el, we found that culturing Nog;Grem1 double-mutant embryos with dorsomorphin restores sclerotome, wh

297 Treatment of vhl(-/-) mutant embryos with HIF2alpha-specific inhibitors downre

298 Proto-HLBs also transiently form in mutant embryos with the histone locus deleted.

299 In mutant embryos with the most severe morphological defect

300 The ability to create large numbers of mutant embryos without inbred lines opens exciting new p