ライフサイエンスコーパス: embryonic lethality

1 xpression can cause developmental defects or embryonic lethality.

2 cell coverage of the vasculature leading to embryonic lethality.

3 n mammalian skin, are yet unknown because of embryonic lethality.

4 ar uptake of the TC-bound B12, do not confer embryonic lethality.

5 AP/TAZ leads to impaired vascularization and embryonic lethality.

6 he TRP channel TRPM7, which results in early embryonic lethality.

7 hat loss of functional Zbtb24 leads to early embryonic lethality.

8 ection of AAV9-sgRNAs, thereby circumventing embryonic lethality.

9 ce results in right ventricle hypoplasia and embryonic lethality.

10 k efficient centriole conversion and lead to embryonic lethality.

11 tical for life, because its absence leads to embryonic lethality.

12 In mice, global deficiency causes embryonic lethality.

13 pression of spontaneous cell death, and post-embryonic lethality.

14 n addition, capzb over-expression results in embryonic lethality.

15 nockout of Specc1l in mouse results in early embryonic lethality.

16 ntegrity, leading to osmotic sensitivity and embryonic lethality.

17 how that Slc52a3 deficiency results in early embryonic lethality.

18 s to delayed initiation of cell division and embryonic lethality.

19 strated that deletion of Ada3 leads to early embryonic lethality.

20 ortic valve, ventricular septal defects, and embryonic lethality.

21 leads to developmental retardation and early embryonic lethality.

22 the endothelium because this ablation causes embryonic lethality.

23 generation of mature blood cells, leading to embryonic lethality.

24 ed EGFR nulls, an AGR2 null also resulted in embryonic lethality.

25 m-line elimination of the Ubiad1 gene caused embryonic lethality.

26 postimplantation stage, which leads to early embryonic lethality.

27 leads to chromosome segregation defects and embryonic lethality.

28 egregating variants modify the penetrance of embryonic lethality.

29 HR gene (Fancd2) and Polq in mice results in embryonic lethality.

30 Shox2 expression from the developing SAN and embryonic lethality.

31 apitulate the same severe heart phenotype or embryonic lethality.

32 al, vascular and heart defects, resulting in embryonic lethality.

33 defects of Rif1-depleted ESCs and associated embryonic lethality.

34 suppresses developmental defects and rescues embryonic lethality.

35 romatin structure, DNA damage, apoptosis and embryonic lethality.

36 enotype, depletion of the stem cell pool and embryonic lethality.

37 g a molecular explanation for htt(-/-) early embryonic lethality.

38 d completely normal except for modest (~15%) embryonic lethality.

39 sed MPI defects, FOA, oocyte aneuploidy, and embryonic lethality.

40 e and severity of NTDs that led to increased embryonic lethality.

41 e (HD), while htt(-/-) mutants display early embryonic lethality.

42 Vitamin E (VitE) deficiency results in embryonic lethality.

43 oedema, haemorrhage and increased levels of embryonic lethality.

44 stemic knock-out of Palb2 in mice results in embryonic lethality.

45 fects, upregulation of Tbx5 target genes and embryonic lethality.

46 es including dwarfism, anophthalmia, and 80% embryonic lethality.

47 rates and litter sizes argue against induced embryonic lethality.

48 eptor agonist to pregnant dams rescued early embryonic lethality.

49 rdination results in abnormal cell shape and embryonic lethality.

50 Mendelian genotype distribution, suggesting embryonic lethality.

51 s to complex developmental defects and early embryonic lethality.

52 e genes can lead to growth abnormalities and embryonic lethality.

53 and germ-line deletion of Palb2 led to early embryonic lethality.

54 timately collapse, leading to hemorrhage and embryonic lethality.

55 ess, and, in mice, manifests with very early embryonic lethality.

56 d Nodal signaling, gastrulation failure, and embryonic lethality.

57 (cFlip(fl/fl) VillinCre(+) mice) resulted in embryonic lethality.

58 ic loss-of-function of YY1 resulted in early embryonic lethality.

59 deletion of many SR protein genes results in embryonic lethality.

60 on in mma-1 animals causes larval arrest and embryonic lethality.

61 h10 loss-of-function mutations lead to early embryonic lethality.

62 type; the Rala null leads to exencephaly and embryonic lethality.

63 Germ line deletion of RHAU led to embryonic lethality.

64 etardation, delayed hindbrain formation, and embryonic lethality.

65 ndent manner, and a mouse knock-out leads to embryonic lethality.

66 exocytosis and cytokinesis, leading to early embryonic lethality.

67 incompletely penetrant temperature-sensitive embryonic lethality.

68 wild type, chr12 chr23 double mutants cause embryonic lethality.

69 tion, whereas homozygous mutations result in embryonic lethality.

70 show severe defects in heart development and embryonic lethality.

71 mbined lipin-1 and lipin-2 deficiency caused embryonic lethality.

72 Higher doses of morpholino induce embryonic lethality.

73 ensable, given that Atad5 knock-out leads to embryonic lethality.

74 nockdown of S18-2 in zebrafish larvae led to embryonic lethality.

75 and poorly developed OFT resulting in early embryonic lethality.

76 ts in deficient vascular development causing embryonic lethality.

77 vation of developmental genes and subsequent embryonic lethality.

78 matheca, which disrupts ovulation and causes embryonic lethality.

79 and cardiac muscle defects, leading to early embryonic lethality.

80 d Sax, and elevated Dpp signaling results in embryonic lethality.

81 h sacs/primordial thoracic ducts, oedema and embryonic lethality.

82 lines in order to investigate the causes of embryonic lethality.

83 ryos markedly more susceptible than males to embryonic lethality.

84 ed, cause severe developmental phenotypes or embryonic lethality.

85 lar non-compaction cardiomyopathy (NCC) with embryonic lethality.

86 ln and p.Thr343Met variants failed to rescue embryonic lethality.

87 e total body deletion in mice leads to early embryonic lethality.

88 ts necessity in adult HSCs is unknown due to embryonic lethality.

89 te SM22-Cre: SCAP(flox/flox) genotype due to embryonic lethality.

90 ut of both paralogs in mice results in early embryonic lethality.

91 d specification of mesendoderm, resulting in embryonic lethality.

92 ic progenitor cells, resulting in anemia and embryonic lethality.

93 iotropic developmental phenotypes, including embryonic lethality.

94 K-Ras(G12V) from the K-Ras locus resulted in embryonic lethality.

95 ormation of abnormal actin bundles and early embryonic lethality.

96 neuronal apoptosis, which eventually lead to embryonic lethality.

97 ogaster crossed to uninfected females causes embryonic lethality.

98 e that lack caspase-8 display MLKL-dependent embryonic lethality(4), as do mice that express catalyti

99 t a lack of distinct PcG proteins results in embryonic lethality accompanied by differentiation biase

100 inting, persist in these embryos, leading to embryonic lethality after implantation.

101 ice harboring an Emu-Myc transgene displayed embryonic lethality, allelic loss of Bif-1 dramatically

102 e activity also prevented Ripk1(D325A/D325A) embryonic lethality, although the mice died before weani

103 that SirT7-knockout mice suffer from partial embryonic lethality and a progeroid-like phenotype.

104 zyme critical in microRNA biogenesis, causes embryonic lethality and activation of the p53 pathway.

105 nt and vessel formation and function lead to embryonic lethality and are important in the pathogenesi

106 identifies transcriptional events underlying embryonic lethality and associates previously uncharacte

107 ciated with significant phenotypes including embryonic lethality and cancer.

108 urthermore, Commd9 deletion in mice leads to embryonic lethality and complex cardiovascular alteratio

109 ementation of selected n-6 PUFAs rescued the embryonic lethality and defective permeability barrier.

110 Second, although loss of 53BP1 rescues the embryonic lethality and HR defects in BRCA1-deficient mi

111 the morula stage and demonstrating elevated embryonic lethality and involvement of TSPO in embryonic

112 s the mir-35-42 mutant phenotype by inducing embryonic lethality and low fecundity.

113 ors result in CED-3-dependent suppression of embryonic lethality and meiotic chromosome non-disjuncti

114 ulates features of Meckel syndrome including embryonic lethality and multiorgan defects.

115 omeostasis but additionally results in early embryonic lethality and neural tube closure defects.

116 Cwc27 mutant mouse models, with significant embryonic lethality and severe phenotypes in the complet

117 To avoid early embryonic lethality and study NFP function in later card

118 did not affect ILK localization to FAs, the embryonic lethality and the in vitro migration defects a

119 -specific knockouts also did not exhibit any embryonic lethality and were viable to adulthood.

120 utants have impaired mitochondrial function, embryonic lethality, and agenesis of the liver.

121 s, but instead causes proliferation defects, embryonic lethality, and dysregulation of ESC signaling

122 ral cell migration, differentiation, partial embryonic lethality, and hemorrhaging were observed afte

123 of the genes coding for RNase H2 results in embryonic lethality, and in humans, RNase H2 hypomorphic

124 crossing suggested that CEK4 knockout causes embryonic lethality, and microscopy analysis of the abor

125 efects in dystroglycan glycosylation, avoids embryonic lethality, and produces a phenotype resembling

126 of SRSF2 in the hematopoietic lineage caused embryonic lethality, and Srsf2-deficient fetal liver cel

127 at disruption of both CRTC2 and CRTC3 causes embryonic lethality, and that a single allele of either

128 ead to degradation of type I collagen, early embryonic lethality, and the scarcity of reported osteog

129 CMP-sialic acid synthase (CMAS) resulted in embryonic lethality around day 9.5 post coitum (E9.5) in

130 iosus, reduced myocardial proliferation, and embryonic lethality around E13.

131 of loss of SNX14 in mice, which resulted in embryonic lethality around mid-gestation due to placenta

132 of Gata4 in hepatic mesenchymal cells led to embryonic lethality around mouse embryonic stage 13.5, l

133 Genetic deletion of Casp8 results in embryonic lethality as a result of uncontrolled necropto

134 A lipodystrophy allele of seip-1 resulted in embryonic lethality as well and could be rescued by PUFA

135 o known as Trp53), revealed late-gestational embryonic lethality associated with a host of phenotypes

136 iency, Paxx/Xlf double-knockout mice display embryonic lethality associated with genomic instability,

137 ctivated kinase 4 (PAK4) in the mouse causes embryonic lethality associated with heart and brain defe

138 deletion of alpha-pv in mice results in late embryonic lethality associated with hemorrhages and redu

139 ivation of Atm and H2ax in mice causes early embryonic lethality associated with substantial cellular

140 ormalities, homozygous deficiency results in embryonic lethality at approximately embryonic day 7.

141 shown that Foxo1 knockout in mice results in embryonic lethality at E11 because of impaired vascular

142 study showed that Sag total knockout caused embryonic lethality at E11.5-12.5 days with associated d

143 and arteriovenous malformations, leading to embryonic lethality at E12.5.

144 Disruption of Drosha in VSMCs resulted in embryonic lethality at E14.5 with severe liver hemorrhag

145 own of tbeta4 has been reported to result in embryonic lethality at E14.5-16.5, with severe cardiac a

146 tion of mouse tropomodulin3 (Tmod3) leads to embryonic lethality at E14.5-E18.5, with anemia due to d

147 rt that Sag endothelial deletion also causes embryonic lethality at E15.5 with poor vasculogenesis.

148 that ablation of the mouse Brpf1 gene causes embryonic lethality at E9.5.

149 of Cdc42 in mice has been shown to result in embryonic lethality at embryonic day 6.5 (E6.5) before b

150 lacking FLRT2 in endothelial cells exhibited embryonic lethality at mid-gestation, with systemic cong

151 rturbed vascular development, hemorrhage and embryonic lethality at mid-gestation.

152 irected deficiencies of Cx45 in mice lead to embryonic lethality attributable to morphological and fu

153 BMP10 deletion in mice results in embryonic lethality because of impaired cardiac developm

154 Absence of ALK5 leads to early embryonic lethality because of severe defects in vascula

155 zygous deletion of Letm1 in mice resulted in embryonic lethality before day 6.5 of embryogenesis and

156 e UTX KO mice, which lack the UTY gene, show embryonic lethality before embryonic day 11.5.

157 r specifically in cardiomyocytes resulted in embryonic lethality before embryonic day 12.5.

158 melastatin-like 7 (Trpm7) in mice results in embryonic lethality before embryonic day 7.

159 TSPCs impairs their self-renewal, leading to embryonic lethality before embryonic day 9.0, a developm

160 of both alleles of PRKCSH in mice results in embryonic lethality before embryonic day E11.5.

161 ine kinases 1 and 2 (Sphk1 and Sphk2) showed embryonic lethality between E11.5 and E12.5 due to defec

162 d-ligation defects and p53- and Ku-dependent embryonic lethality, but open hairpin-sealed ends normal

163 pment in mice resulted in p53 activation and embryonic lethality, but the mice with arf-bp1 deletion

164 Inactivation of Dnmt3b results in mouse embryonic lethality, but which activities are involved i

165 the global deletion of Etv2 and that it has embryonic lethality by embryonic day 9.5.

166 pathy, and homozygous expression resulted in embryonic lethality by midgestation.

167 Vinculin loss results in embryonic lethality, cardiovascular diseases, and cancer

168 ion in rod bipolar cells, thereby overcoming embryonic lethality caused by germline Frmpd1 deletion.

169 have shown that MLKL deficiency rescued the embryonic lethality caused by loss of Caspase-8 or FADD.

170 TRPM7 expression, indicating that the early embryonic lethality caused by loss of hepatocystin is ma

171 Moreover, the embryonic lethality caused by the deficiency of mdm2 was

172 al of paternal mitochondria causes increased embryonic lethality, demonstrating that PME is important

173 GRK2 null animals exhibit embryonic lethality due to a severe developmental heart

174 ial-specific WNK1 gene disruption results in embryonic lethality due to angiogenic and cardiovascular

175 rmined that loss of USP22 in mice results in embryonic lethality due to defects in extra-embryonic pl

176 Unexpectedly, male UTX-null mice escape embryonic lethality due to expression of UTY, a paralog

177 Loss of murine Nf1 results in embryonic lethality due to heart defects, while mice wit

178 icult because global Met knockout results in embryonic lethality due to placental and liver abnormali

179 rated in EPCR knockout mice which show early embryonic lethality due to placental thrombosis.

180 etal liver, erythroid maturation arrest, and embryonic lethality due to profound anemia.

181 of Notch1 in Prox1 heterozygous mice rescued embryonic lethality due to Prox1 haploinsufficiency and

182 suggesting that Acer2 deficiency results in embryonic lethality due to the atrophy of the fetal bloo

183 The D325A mutation in mouse RIPK1 leads to embryonic lethality during mouse development(2,3).

184 e to differentiation, which further leads to embryonic lethality early in gestation.

185 he wild type PSTPIP1 in mice lead to partial embryonic lethality, growth retardation, and elevated le

186 report that Naa10-null mice display partial embryonic lethality, growth retardation, brain disorders

187 FOXF1-deficient embryos exhibited embryonic lethality, growth retardation, polyhydramnios,

188 e observed and heterozygous mice also showed embryonic lethality (haploinsufficient lethality) observ

189 Embryonic lethality has limited the characterization of

190 hereas complete loss of Spartan causes early embryonic lethality, hypomorphic mice with low amounts o

191 us variant (such as aneuploidy) could escape embryonic lethality if the genome-wide burden of slightl

192 , a knock-in (KI) Tonsl mouse model leads to embryonic lethality, implying the physiological importan

193 sed imprinted genes, is the primary cause of embryonic lethality in 70-80% of parthenogenotes immedia

194 The finding of early embryonic lethality in a Tonsl(-/-) murine model and the

195 germ line deletion of Flcn results in early embryonic lethality in animal models.

196 expressed by osteoblast-lineage cells; early embryonic lethality in Bag-1 null mice, however, has lim

197 e DNA damage response factor 53BP1 overcomes embryonic lethality in Brca1-nullizygous mice and rescue

198 ortance in development is exemplified by the embryonic lethality in cFLIP-deficient animals.

199 ytoplasmic incompatibility, which results in embryonic lethality in crosses between infected males an

200 Each gene additively augments embryonic lethality in crosses between infected males an

201 We discovered a selfish element causing embryonic lethality in crosses between wild strains of t

202 , we investigated the cellular basis of male embryonic lethality in D. melanogaster induced by Spirop

203 t the dominant inducers of RIP kinase-driven embryonic lethality in FADD-deficient mice.

204 ated thin filament length, were the cause of embryonic lethality in HSPB7 KOs.

205 idgestation, consistent with RTT-linked male embryonic lethality in humans.

206 yeast and causes chromosome instability and embryonic lethality in mammals.

207 th a putative role in splicing, causes early embryonic lethality in mice and that its loss in Purkinj

208 dly, catalytically inactive prostasin caused embryonic lethality in mice lacking its cognate inhibito

209 Ubiquitous inactivation of Utf1 causes embryonic lethality in mice with a hybrid genetic backgr

210 by REMOTE-control was potent enough to cause embryonic lethality in mice, reminiscent of a genetic kn

211 Because complete absence of MESD causes embryonic lethality in mice, we hypothesized that the OI

212 both D2899A and Q2740P mutations cause early embryonic lethality in mice, without displaying dominant

213 on, causing right ventricular hypoplasia and embryonic lethality in mice.

214 repair, resulting in cellular senescence and embryonic lethality in mice.

215 alteration of which may be involved in early embryonic lethality in mice.

216 and homozygous loss of this protein leads to embryonic lethality in mice.

217 poplasia (FDH), whereas gene deletion causes embryonic lethality in mice.

218 Disruption of Axin1 causes embryonic lethality in mice.

219 scriptional elongation rate results in early embryonic lethality in mice.

220 stemic gene knockout (KO) of Anp32b leads to embryonic lethality in mice.

221 ted in yeast but Rev3l disruption results in embryonic lethality in mice.

222 or subunit, and knockout of Med31 results in embryonic lethality in mice; however, Med31 function in

223 rd, homozygous deletion of CK2alpha leads to embryonic lethality in mid-gestation potentially due to

224 its catalytic subunit (P4ha1(-/-)) leads to embryonic lethality in mouse, whereas P4ha1(+/-) mice ha

225 While the function of this gene is unknown, embryonic lethality in Mrpl3 knock-out mice suggests it

226 Molecular strategies that promote embryonic lethality in these agricultural pests are limi

227 developmental arrest in frogs and zebrafish, embryonic lethality in transgenic mice, and lesions in m

228 o the inhibition of cell death and increased embryonic lethality in unirradiated animals.

229 cell cycle progression and results in early embryonic lethality in vertebrates.

230 described, and murine Nmnat1 knockouts show embryonic lethality, indicating that complete absence of

231 affects endogenous geminin levels; apparent embryonic lethality is observed around 3-4 hours after m

232 Although ablation of Zfp516 causes embryonic lethality, knockout embryos still show drastic

233 Interestingly, the maternal-effect embryonic lethality, larval lethality, and adult eye def

234 ent to yield homozygous mutant mice revealed embryonic lethality later than occurred with global Gata

235 though NIR deficiency in mice leads to early embryonic lethality, lymphoid-restricted deletion result

236 tKO mice demonstrate partial embryonic lethality, most likely due to the role of miR-

237 th syndromes (i.e. ribosomal frame-shifting, embryonic lethality, neurodegeneration and cancer) typic

238 e TGF-beta1(Lbeta3/Lbeta3) mice show neither embryonic lethality nor signs of multifocal inflammation

239 Here we show that embryonic lethality observed in abp1-1, which has been a

240 unrecognized action of Meis1 may explain the embryonic lethality observed in Meis1(-/-) mice that ari

241 n a weak ced-3(-) mutant, and suppresses the embryonic lethality of a mutant defective for the apopto

242 PE1 in CSR has been difficult because of the embryonic lethality of APE1 ablation in mice.

243 We demonstrate that the embryonic lethality of aph-1(zu147) mutants can be suppr

244 In contrast to the early embryonic lethality of Atm(KD/KD) mice, AtmR3016H (Atm(R

245 whose aberrant up-regulation contributes to embryonic lethality of Dnmt3b knockout embryos.

246 Here, we bypassed the embryonic lethality of dually PARP-1/PARP-2-deficient mi

247 hampered by the lack of animal models due to embryonic lethality of GPI biosynthesis gene null mutant

248 In contrast to the early embryonic lethality of H2AX(-/-)XLF(-/-) mice, 53BP1(-/-

249 n Bcl-xL has remained unclear because of the embryonic lethality of mice globally deleted for Bcl-xL.

250 a role in patterning blood formation, early embryonic lethality of mice lacking Hh signaling preclud

251 p53 deletion prevents the embryonic lethality of normal tissues lacking Mdm2, sugg

252 ntial role in development, apparent from the embryonic lethality of Pbmr1-null mice, but very little

253 etween Stx1 isoforms Stx1A and Stx1B and the embryonic lethality of Stx1A/1B double knock-out (DKO) m

254 We report the first characterization of the embryonic lethality of the Apj-/- mice.

255 Early embryonic lethality of the mouse knockout challenges inv

256 f TRPM7 in mouse models has been hampered by embryonic lethality of transgenic ablations.

257 Thus, embryonic lethality of Ubiad1 deficiency results from de

258 ypes in homozygotes: skin abnormalities, and embryonic lethality on normal chow diet, but not on high

259 es viability of the individual (for example, embryonic lethality) or results in profound loss of fitn

260 versican expression loss in mice results in embryonic lethality owing to cardiovascular defects.

261 eas complete ATR pathway inactivation causes embryonic lethality, partial Hus1 impairment has been ac

262 While TDP-43 knockout mice show early embryonic lethality, post-natal conditional knockout mic

263 use model and found that loss of Fdxr led to embryonic lethality potentially due to iron overload in

264 Deletion of CDK2AP1 leads to early embryonic lethality, potentially through altered differe

265 e perinatal lethal, in contrast to the early embryonic lethality previously reported for Rnaseh2b- or

266 h GATA genes, but not either alone, leads to embryonic lethality prior to the onset of their expressi

267 ate, whereas deletion from mice causes early embryonic lethality, raising the question of whether La

268 To circumvent the embryonic lethality resulting from Cx45 deficiency, mice

269 The embryonic lethality resulting from loss of SEC24C occurs

270 ion of Rspo3 in the Isl1 lineage resulted in embryonic lethality secondary to impaired development of

271 ed in a Drosophila tetracycline-suppressible embryonic lethality system by analyzing the frequency an

272 te for the lack of TFPI and rescue TFPI-null embryonic lethality, Tfpi(+/-) mice lacking the platelet

273 cytes of maternal-zygotic mutants results in embryonic lethality that can be fully rescued with gdf3

274 Loss of schizo caused embryonic lethality that could be rescued to 2(nd) insta

275 nstitutive expression of MDM2 I438K leads to embryonic lethality that is rescued by p53 deletion, sug

276 or survival of mouse embryos, but because of embryonic lethality, their precise developmental roles r

277 Gata4(MyoDel/wt);Tbx5(+/-) mice displayed embryonic lethality, thin myocardium with reduced cell p

278 Embryonic lethality was completely prevented by the comb

279 Embryonic lethality was prevented by inactivation of RIP

280 DNase II-dependent embryonic lethality was rescued by loss of STING functio

281 To bypass embryonic lethality we used Tie2CRE-mediated recombinati

282 e/lox-specific deletion to prevent double-KO embryonic lethality, we developed two mouse models of a

283 use complete ATR pathway inactivation causes embryonic lethality, we weakened the ATR mechanism to di

284 which if mutated (or knocked-out) result in embryonic lethality when homozygous, and initiate the st

285 nes that are widely expressed or which cause embryonic lethality when mutated.

286 tion of the editing activity of AlaRS caused embryonic lethality, whereas an intermediate reduction i

287 Ssb1/Ssb2 double knockout (DKO) caused early embryonic lethality, whereas conditional Ssb1/Ssb2 doubl

288 nstitutive knockout of Lkb1 in mice leads to embryonic lethality, whether Lkb1 is required for the gr

289 omozygous seip-1 mutants displayed penetrant embryonic lethality, which is caused by the disruption o

290 Ezh2 in developing mouse endothelium caused embryonic lethality with compromised vascular integrity

291 hat the inactivation of Cdc42 in NCCs caused embryonic lethality with craniofacial deformities and ca

292 pk as a model for Shh dysfuction) results in embryonic lethality with e12.5 embryos having exencephal

293 e show that disruption of L3mbtl2 results in embryonic lethality with failure of gastrulation.

294 Embryonic lethality with incomplete penetrance was obser

295 deletion of ERG (Erg(cEC-KO)) in mice causes embryonic lethality with vascular defects.

296 The deletion of Cdc42 in ECs caused embryonic lethality with vasculogenesis and angiogenesis

297 specific deletion of Wnk1 in mice results in embryonic lethality, with angiogenesis and cardiac defec

298 ion of ARID1a-DNA binding in mice results in embryonic lethality, with mutant embryos manifesting pro

299 t together with Atm loss resulted in partial embryonic lethality, with the surviving double-mutant mi

300 ac trabeculation, cause cardiomyopathies and embryonic lethality, yet how tissue symmetry is broken t