Analysis Tools
mortality/aging
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• homozygous mutant embryos were already under-represented and developmetally retarded at E11.5
• no mutant embryos were retrieved after E13.5
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cardiovascular system
| N |
• at E9.0-9.5, homozygous mutant embryos appeared grossly normal with regularly beating hearts and visible blood in their circulation
• at E9.0-9.5, the dorsal aorta, intersomitic vessels and branching head veins of mutant embryos proper appeared histologically normal
• also, at E9.0-9.5, yolk sac-derived embryonic red blood cells were present in the mutant blood vessels
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• as early as E9.5, 65% of homozygous mutant embryos (designated type I mutants) displayed yolk sacs that lacked branching vitelline vessels, and formed a honeycomb-like network of interconnecting sinusoids instead
• at E9.5, approximately 35% of homozygous mutant embryos (designated type II mutants) exhibited normal-appearing yolk sac vitelline vessels
• by E10, both type I and type II mutants lacked normal vitelline vessels
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• by E10.5, about two-thirds of all mutant embryos were growth-retarded, highly necrotic, and displayed an enlarged pericardial sac; this most likely reflects the fraction of type I mutants that failed to develop normal yolk sac vasculature at E9.5
• the remaining one-third of embryos, presumably type II mutants, lost the vitelline vessels completely and exhibited the same honeycomb-like vasculature as type I mutants
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embryo
| N |
• at E9.0-9.5, the number of somites and appearance of the cranial prominence were unaffected
• at E9.0-9.5, placento-allantoid fusion appeared normal
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• as early as E9.5, 65% of homozygous mutant embryos (designated type I mutants) displayed yolk sacs that lacked branching vitelline vessels, and formed a honeycomb-like network of interconnecting sinusoids instead
• at E9.5, approximately 35% of homozygous mutant embryos (designated type II mutants) exhibited normal-appearing yolk sac vitelline vessels
• by E10, both type I and type II mutants lacked normal vitelline vessels
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• at E10, type II embryos were also developmentally less severely retarded than type I embryos correlating with a later onset of the yolk sac blood vessel defect
• by E10.5, all homozygous embryos were grossly abnormal: about two-thirds of all embryos were severely growth-retarded
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• at E9.0, mutant yolk sacs developed ample sinusoidal spaces, and blood islands with lumens similar in diameter to wild-type, and containing pooled primitive red cells; however, larger lumens were absent in mutant yolk sacs
• notably, endodermal and endothelial cells lining the sinusoids in mutant yolk sacs appeared normal
• the total number and content of the erythroid, macrophage and mixed colonies derived from precursors present in mutant yolk sacs did not differ from control littermates
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growth/size/body
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• at E10, type II embryos were also developmentally less severely retarded than type I embryos correlating with a later onset of the yolk sac blood vessel defect
• by E10.5, all homozygous embryos were grossly abnormal: about two-thirds of all embryos were severely growth-retarded
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