Analysis Tools
mortality/aging
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• homozygous mutant embryos die at around E10.5-E11.5
• at E10.5, ~15% of homozygotes are completely resorbed, ~75% are arrested midway in the turning process while the remaining (<10%) show relatively normal body structures
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embryo
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• at E9.5, homozygotes display defects in yolk sac angiogenesis, with large pools of blood abnormally accumulated in some regions
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• at E9.5, mutant yolk sacs lack distinct blood vessels despite the presence of endothelial cells
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• at E9.5, homozygotes display a disorganized vascular plexus in the brain region
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• at E9.5, ~75% of homozygotes are arrested midway in the turning process; the remaining 25% exhibit normal turning
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• at E9.5, many severely affected homozygotes exhibit a lateral spreading of the ventral mesoderm
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• at E9.5, homozygotes display variable distortion of the posterior region
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• at E9.5, homozygotes appear developmentally retarded relative to wild-type embryos
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• at E8.5 (but not earlier), homozygous mutant embryos are smaller than wild-type embryos
• by E10.5, 75% of mutant embryos are much smaller than wild-type embryos
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pale yolk sac
(
J:53289
)
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• at E9.5, mutant yolk sacs are generally pale
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• in vitro, mutant yolk sacs contain twice as many myeloid colony-forming units as wild-type yolk sacs
• however, no change in the number of erythroid precursor cells is observed, suggesting normal differentiation of hematopoeitic precursors into the erythroid lineage
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• at E8.5, some homozygotes display delayed chorioallantoic fusion relative to wild-type embryos
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• at E9.5, homozygotes exhibit an abnormal, simplified vascular network instead of a branched, tree-like network
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cardiovascular system
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• at E9.5, layers of endothelial cells are often dissociated from mesenchymal cells
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• at E9.5, homozygotes exhibit abnormally enlarged, misshapen blood vessels throughout the embryos instead of normal vasculature
• in addition, mesenchyme is almost absent in severely affected mutants
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• at E9.5, the mutant dorsal aorta is malformed and invades into the ventral region of somites
• at E10.5 and E11.5, endothelial cells of the mutant dorsal aorta are surrounded by a thin, disorganized smooth muscle layer
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• in vitro, homozygous mutant embryos are unable to direct the organization of endothelial cells into a network of tubes radiating away from the embryo, indicating an angiogenic defect
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• at E9.5, homozygotes display defects in yolk sac angiogenesis, with large pools of blood abnormally accumulated in some regions
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• at E9.5, mutant yolk sacs lack distinct blood vessels despite the presence of endothelial cells
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• at E9.5, homozygotes display a disorganized vascular plexus in the brain region
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• at E10.5 and E11.5, endothelial cells of the mutant dorsal aorta are surrounded by a thin, disorganized smooth muscle layer
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hemorrhage
(
J:53289
)
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• at E9.5, homozygotes show abnormal accumulation of blood cells permeating several tissues e.g the brain and limb buds, suggesting that weakened blood vessel walls may have hemorrhaged
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growth/size/body
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• at E9.5, homozygotes appear developmentally retarded relative to wild-type embryos
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• at E8.5 (but not earlier), homozygous mutant embryos are smaller than wild-type embryos
• by E10.5, 75% of mutant embryos are much smaller than wild-type embryos
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nervous system
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• at E9.5, all homozygotes lack an identifiable forebrain
• in contrast, the midbrain region and midbrain-hindbrain boundary appear unaffected
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• at E9.5, severely affected homozygotes display abnormal spinal cord development
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cellular
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• at E9.5, homozygotes display massive apoptosis in the head mesenchyme and somites
• notably, somite apoptosis is most prevalent in the sclerotome region
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muscle
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• at E10.5 and E11.5, endothelial cells of the mutant dorsal aorta are surrounded by a thin, disorganized smooth muscle layer
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skeleton
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• at E9.5, homozygotes display a severly reduced sclerotomal region
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hematopoietic system
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• in vitro, mutant yolk sacs contain twice as many myeloid colony-forming units as wild-type yolk sacs
• however, no change in the number of erythroid precursor cells is observed, suggesting normal differentiation of hematopoeitic precursors into the erythroid lineage
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