Analysis Tools
mortality/aging
|
• homozygotes are present at the expected Mendelian frequency (25%) up to E9.5
• however, viable mutant embryos are obtained at a reduced frequency from E10.5 (18.8%) to E11.5 (4.1%), until all are dead by E12.5 probably as a result of heart failure
|
growth/size/body
|
• at E11.5, ~80% of homozygotes appear underdeveloped and growth retarded relative to wild-type embryos, despite normal placental development and absence of excessive apoptosis or reduced cellular proliferation
|
|
• at E11.5, ~80% of homozygotes are smaller in size relative to wild-type embryos
|
cardiovascular system
|
• at E10.5, mutant embryos with a thin ventricular myocardium exhibit poor inner trabeculation
• in contrast, endocardial cushions appear unaffected
|
|
• at E10.5, ~80% of mutant embryos display a thinner ventricular myocardium than wild-type embryos
|
|
• ~50% of mutant embryos surviving at E11.5 exhibit signs of abdominal hemorrhage, despite normal development of the vascular endothelium
|
cellular
|
• mutant embryonic fibroblast cells show impaired apoptosis-inducing signaling by Fas, Tnfrsf1a, and Tnfrsf25 (also known as death receptor 3, DR3)
• in contrast, no differences are observed in DR4-, oncogene (E1A and Myc)- or drug (adriamycin)- induced apoptosis relative to wild-type cells
|
muscle
|
• at E10.5, mutant embryos with a thin ventricular myocardium exhibit poor inner trabeculation
• in contrast, endocardial cushions appear unaffected
|
|
• at E10.5, ~80% of mutant embryos display a thinner ventricular myocardium than wild-type embryos
|
embryo
|
• at E11.5, ~80% of homozygotes appear underdeveloped and growth retarded relative to wild-type embryos, despite normal placental development and absence of excessive apoptosis or reduced cellular proliferation
|
|
• at E11.5, ~80% of homozygotes are smaller in size relative to wild-type embryos
|
