Analysis Tools
mortality/aging
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• homozygous mutant embryos are recovered at the expected Mendelian frequencies at E8.5, E9.5, and E10.5, but are completely lost by E11.5
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growth/size/body
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• by E10.5, homozygotes display severe growth retardation relative to wild-type controls
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• as early as E9.5, mutant embryos are significantly smaller than wild-type embryos
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microcephaly
(
J:82356
)
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• at E9.5, homozygotes exhibit a reduced head size
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cardiovascular system
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• at E9.5, mutant yolk sacs display a discontinuity in endothelial cells
• by E10.5, endothelial cells are detached from subjacent mesoepithelium
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• at E9.0, mutant yolk sac vessels exhibit a 58% increase in the number of endothelial cells per millimeter of vessel length, as determined by Ki67 staining
• however, no difference in endodermal cell numbers is observed
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• at E9.0, enlarged intersomitic networks and dorsally fused intersomitic vessels are observed
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• at E9.0, mutant yolk sacs show a slight decrease in the number of pericytes (PCs) relative to wild-type yolk sacs
• at E9.0, mutant yolk sacs exhibit round and sparsely distributed PCs between the endoderm and endothelium
• by E9.5, mutant PCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in yolk sacs
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• at E8.25-E9.0, homozygotes display vascular development defects, including a poorly formed cerebral vascular plexus
• at E9.0, a narrow dorsal aorta, enlarged intersomitic networks, and dorsally fused intersomitic vessels are observed
• at E9.5, homogeneously enlarged primitive vessels defective in vascular remodeling and branching, and impaired pericyte investment adjacent to endothelial structures are observed
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• at E9.0, homozygotes display a collapsed dorsal aorta which includes abundant endothelial cells and disorganized intersomitic sprouts
• at E9.5-E10.5, the dorsal aorta is atrophic and resembles a disorganized string of aligned endothelial cells with fewer intersomitic sprouts; by E10.5, its outline is discontinuous
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• at E9.5, homozygotes show absence of large branching vessels, and accumulation of primitive blood cells in the yolk sac
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• at E9.5-E10.5, mutant cerebral vessels lack branching vessels of large diameters
• by E10.5, mutant peripheral vessels are oversized, disorganized, and densely interconnected
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• at E9.5, homozygotes display accumulation of primitive blood cells in the yolk sac
• as early as E8.25, homozygotes display focally enlarged and fused yolk sac vessels
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• at E9.0, mutant yolk sacs exhibit round and sparsely distributed vSMCs between the endoderm and endothelium
• by E9.5, mutant vSMCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in mutant yolk sacs
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• at E9.0, mutant yolk sacs show a slight decrease in the number of vSMCs relative to wild-type yolk sacs
• only a few vSMCs are detected around the mutant dorsal aorta
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• at E9.5, homozygotes exhibit disorganized myocardial trabeculation, lacking finger-like trabeculae lined by endocardial cells
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• at E9.5, the thickness of the myocardial wall is reduced while the space between the endocardium and myocardium is increased
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• at E9.5, mutant developing hearts lacked mesenchymal cushion formation adjacent to the atrioventricular canal
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• at E8.25, homozygotes exhibit delayed cardiac looping relative to wild-type controls
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• at E9.0, homozygotes display abnormal endocardial projections extending beyond the cardiac jelly
• at E9.5, a less intricately folded endocardium, and scattered, disconnected endocardial cells are observed
• mutant endocardial cells exhibit a rounded and shortened morphology relative to wild-type endocardial cells
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• at E9.5, homozygotes display an enlarged pericardial cavity
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• at E9.5, homozygotes display a distended pericardium
• by E10.5, a prominent extension of the pericardial sac is observed
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embryo
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• at E9.5, homozygotes display accumulation of primitive blood cells in the yolk sac
• as early as E8.25, homozygotes display focally enlarged and fused yolk sac vessels
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• by E10.5, homozygotes display severe growth retardation relative to wild-type controls
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• as early as E9.5, mutant embryos are significantly smaller than wild-type embryos
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• at E9.0, mutant yolk sac vascular networks exhibit homogeneously sized and focally enlarged endothelial vessels, instead of a differentiated vasculature composed of large- and small-diameter vessels of interconnecting cells
• at E9.5-E10.5, mutant yolk sac vessels fail to mature and to form large vitelline vessels and a capillary network; instead, endothelial structures are abnormally expanded and fused and a few avascular areas are observed between vessels
• at E9.0, vitelline vessels are reduced in number but display an increase in the % of total vessels of larger diameters (>800 m2)
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muscle
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• at E9.0, mutant yolk sacs exhibit round and sparsely distributed vSMCs between the endoderm and endothelium
• by E9.5, mutant vSMCs are poorly elongated, fail to encircle the endothelial vessels, and are loosely associated with the endothelium in mutant yolk sacs
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• at E9.0, mutant yolk sacs show a slight decrease in the number of vSMCs relative to wild-type yolk sacs
• only a few vSMCs are detected around the mutant dorsal aorta
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• at E9.5, homozygotes exhibit disorganized myocardial trabeculation, lacking finger-like trabeculae lined by endocardial cells
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• at E9.5, the thickness of the myocardial wall is reduced while the space between the endocardium and myocardium is increased
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