mortality/aging
• mutant embryos die at or around E11.5, putatively due to a failure in heart morphogenesis
• however, at E9.5, mutant embryos are indistinguishable from wild-type controls
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cardiovascular system
• at E10.5, morphogenesis of blood vessels leading to and from the heart appears to be abnormal
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• at E10.5, yolk sac vasculature is reduced
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• at E10.5, the common atrial chamber appears to be collapsed and no asymmetric restructuring of the sinus venosus is observed
• endothelial cells in the atrial and ventricular walls appear to lose their integrity by E10.5, and are delaminated at E11.5
• at E11.5, large accumulations of nucleated erythroid cells are found within the heart chambers and blood vessels
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• at E10.5, the asymmetric restructuring of the sinus venosus fails to occur
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hemorrhage
(
J:74966
)
• at E10.5, mutant embryos are still alive but display hemorrhaging into the space between the embryo and the amnion
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embryo
• at E10.5, yolk sac vasculature is reduced
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• by E11.5, an increased number of apoptotic cells is detected among the migrating neural crest population from the trigeminal ganglion and within the adjacent fourth ventricle
• at this stage, mutant neural crest cells no longer exhibit a morphology typical of migrating cells
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hematopoietic system
• at E11.5, a large accumulation of nucleated erythroid cells is observed within the heart chambers, blood vessels, and developing liver
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cellular
• by E11.5, an increased number of apoptotic cells is detected among the migrating neural crest population from the trigeminal ganglion and within the adjacent fourth ventricle
• at this stage, mutant neural crest cells no longer exhibit a morphology typical of migrating cells
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