ライフサイエンスコーパス: mutant embryo

1 RINKLED 1 is upregulated in the e2fab double mutant embryo.

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

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

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

5 ignalling appears to underlie exencephaly in mutant embryos.

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

7 in the developing palatal mesenchyme in Pax9 mutant embryos.

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

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

10 transcripts are dramatically reduced in lis1 mutant embryos.

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

12 arly olfactory neural progenitors in neurog1 mutant embryos.

13 istry similar to that characterized in Dact1 mutant embryos.

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

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

16 ased apoptosis in neural crest structures in mutant embryos.

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

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

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

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

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

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

23 defects in ctr9 morphant and paf1(aln(z24)) mutant embryos.

24 npt2a, are significantly affected in entpd5 mutant embryos.

25 incisor epithelium of both Ikkalpha and Irf6 mutant embryos.

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

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

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

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

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

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

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

33 ated by the partially penetrant lethality of mutant embryos.

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

35 auses the abnormal apical cell shapes in sdk mutant embryos.

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

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

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

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

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

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

42 changes in chromatin accessibility in Sd/Sd mutant embryos.

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

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

45 tify proteins that are misexpressed in dfmr1 mutant embryos.

46 cell alignment and migration paths in vangl2 mutant embryos.

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

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

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

50 HSPC markers in the HE and CHT in plcg1(-/-) mutant embryos.

51 the reduction in NOTCH-related genes in the mutant embryos.

52 protein gene expression in Schwann cells of mutant embryos.

53 ues defective directed cell migration in fz7 mutant embryos.

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

55 oth constitutive and striatal-specific Nolz1 mutant embryos.

56 iminated the residual denticles found in svb mutant embryos.

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

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

59 otide synthesis and energy production in the mutant embryos.

60 filaments and M-lines in slow fibers of the mutant embryos.

61 hypertrophy of sympathoadrenal cells in nf1 mutant embryos.

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

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

64 ained an altered expression pattern in Abph2 mutant embryos.

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

66 expanded the domain of thoracic identity in mutant embryos.

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

68 Mutant embryos additionally feature reduced vSMC coverag

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

70 Wnt1 mutant embryos also have alterations in a hierarchical g

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

72 present in the epaxial region of the double mutant embryos and are able to divide and contribute to

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

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

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

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

77 The smyhc1 mutant embryos and larvae showed reduced locomotion and

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

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

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

81 By analyzing mutant embryos and through targeted genetic perturbation

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

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

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

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

86 errantly expressed throughout the IFE of the mutant embryos, and its forced overexpression mimicked t

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

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

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

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

91 Er71 mutant embryos are nonviable and lack hematopoietic and

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

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

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

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

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

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

98 late defects were observed in the homozygous mutant embryos at multiple stages of development.

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

100 Tendon development was not disrupted in mutant embryos, but shortly after birth tenocytes lost d

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 sult in near-identical NC phenotypes; alyron mutant embryos carrying a null mutation in paf1 were ana

106 the present study, we generated conditional mutant embryos carrying specific inactivation of Onecut

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

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

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

110 the palatal shelves in Med23(fx/fx);Wnt1-Cre mutant embryos compared to controls.

111 intercalary cell behaviors in wild-type and mutant embryos, comparison of temporal dynamics in contr

112 Jabba mutant embryos compensate for this histone deficit by tr

113 Additionally, Drp1 mutant embryos contain lower levels of reactive oxygen s

114 Mutant embryos contain normal numbers of E10.5 intraaort

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

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

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

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

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

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

121 Homozygous mutant embryos develop normally into the mid-juvenile st

122 Mutant embryos develop partially penetrant NTDs while su

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

124 tyly with high penetrance (>95%), and 24% of mutant embryos developed exencephalus, a neural tube clo

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

126 Mutant embryo developmental outcomes are significantly i

127 Mutant embryos did not develop an effective barrier to t

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

129 Chd4 mutant embryos died before birth and exhibited severe ed

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

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

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

133 Mutant embryos display a loss of birefringency in their

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

135 Mutant embryos display accumulation of mesenchymal cells

136 Mutant embryos display epidermal hyperplasia, but also a

137 Mutant embryos display increased levels of acetylated p5

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

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

140 7 hour post fertilization (hpf) MZ ewsa(m/m) mutant embryos displayed a higher incidence of aberrant

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

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

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

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

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

146 elled, we analysed the phenotype of sdk null mutant embryos during Drosophila axis extension using qu

147 Although Pofut2 mutant embryos established anterior/posterior polarity,

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

149 Surprisingly, mutant embryos eventually correct the myocardial deficit

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

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

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

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

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

155 These mutant embryos exhibit fragmented or decondensed nuclei

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

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

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

159 Nisch-mutant embryos exhibited delayed development, characteri

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

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

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

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

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

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

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

167 Mutant embryos failed to establish normal auxin gradient

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

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

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

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

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

173 Mutant embryos had reduced chondrocyte proliferation and

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

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 scxb mutants show no obvious phenotype, scxa mutant embryos have defects in cranial tendon maturation

179 Notably, pMN cells of mutant embryos have elevated Shh signaling, coincident w

180 Our analysis revealed that prdm8 mutant embryos have fewer motor neurons resulting from a

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

182 Med31 mutant embryos have fewer proliferating cells than contr

183 he Fancm gene; similar to MCM mutants, Fancm mutant embryos have increased levels of genomic instabil

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

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

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

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

188 egmentation network, comparing wild-type and mutant embryos in which all graded maternal patterning i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 At E14.5, the number of Thm1;Thm2 double mutant embryos is lower than that for a Mendelian ratio,

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

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

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

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

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

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

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

212 es is essential for maintaining progenitors, mutant embryos lacking the CDK9 kinase component of P-TE

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

214 nd mdm2 were preferentially expressed in the mutant embryos, leading to significant upregulation of t

215 d the domain of WNT response in p120-catenin mutant embryos, like the T domain, is first expanded, an

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

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

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

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

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

221 In Bmp mutant embryos, myocardial differentiation was delayed,

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

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

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

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

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

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

228 In disc1 mutant embryos, proliferating rx3+ hypothalamic progenit

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

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

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

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

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

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

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

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

237 Mutant embryos show Raldh2 downregulation in the lateral

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

239 Mutant embryos showed delayed palate elevation, stage-sp

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

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

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

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

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

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

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

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

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

249 ropic morphological phenotypes in homozygous mutant embryos starting at 3 days post fertilization (dp

250 ctin staining previously observed in Adamts9 mutant embryos, suggest that ADAMTS9 contributes to fibr

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

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

253 6a/Swap70b morphants resemble Ppt/Slb double mutant embryos suggesting that Swap70b and Def6a delinea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 with a model whereby brief exposure of Cdon mutant embryos to ethanol during gastrulation transientl

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

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

277 th up- and down-regulated gene expression in mutant embryos, together with analysis of weak and stron

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

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

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

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

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

283 Mutant embryos up-regulated stress responses at sites of

284 n unbiased chemical screen on zebrafish pkd2 mutant embryos using two publicly available compound lib

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

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

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

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

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

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

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

292 rrangement in both wild-type and snail twist mutant embryos, where our theoretical prediction is furt

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

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

295 catenin is enhanced in Med23(fx/fx);Wnt1-Cre mutant embryos, which, together with downregulation of C

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