Analysis Tools
mortality/aging
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• homozygotes are present at the expected Mendelian ratios up to E9.5, but die between E10.5 and E11.5
• occasional homozygotes are detected at E11.5 but they never survive beyond E12
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growth/size/body
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• many of the mutant embryos display a variable degree of growth retardation at E9.5-E11
• in most cases, reduced embryo size is not linked to a significant reduction in somite number
• occasional mutant embryos are severely developmentally retarded and corresponded to stages 12-36 hrs earlier relative to wild-type embryos
• however, overall early embryonic development and organogenesis appear to occur normally
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embryo
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• many of the mutant embryos display a variable degree of growth retardation at E9.5-E11
• in most cases, reduced embryo size is not linked to a significant reduction in somite number
• occasional mutant embryos are severely developmentally retarded and corresponded to stages 12-36 hrs earlier relative to wild-type embryos
• however, overall early embryonic development and organogenesis appear to occur normally
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• at E10.5, discontinuities or ruptures of basement membranes are observed in mutant extraembryonic tissues
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• at E11.5, the contact between maternal and embryonic blood is reduced
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• at E11.5, the mutant Reichert's membrane appears fragile, thin, and disorganized
• electron-dense string-like structures are shown to be loosely and abnormally arranged at E10
• ruptures cause severe bleeding of maternal blood into the yolk sac cavity, contributing to the death and resorption of mutant embryos
• at multiple sites the contact with the trophectoderm layer and parietal endoderm cells is lost, suggesting defects in cell-matrix interactions
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• thin at E11.5
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• at E11.5, the thickness of the placenta labyrinth layer is reduced
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• at E11.5, the development of the labyrinth layer of the placenta is retarded in mutant embryos relative to wild-type embryos
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cardiovascular system
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• at E11.5, the contact between maternal and embryonic blood is reduced
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• at E10.5-E11.5, mutant embryos display dilated blood vessels
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• at E10.5-E11.5, mutant embryos exhibit bleeding into the pericardium
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nervous system
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• at E11.5, mutant embryos exhibit neuronal ectopias in the brain because of abnormal migration of neuronal cells through the pial basement membrane into the surrounding mesenchymal layers
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homeostasis/metabolism
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• at E10.5-E11.5, mutant embryos exhibit bleeding into the pericardium
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cellular
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• at E11.5, mutant embryos exhibit neuronal ectopias in the brain because of abnormal migration of neuronal cells through the pial basement membrane into the surrounding mesenchymal layers
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• at E10.5, discontinuities or ruptures of basement membranes are observed both in mutant embryos and in extraembryonic tissues
• at E11.5, an increased instability of basement membranes is detected in various tissues
• local disruption of the pial basement membrane is the most likely cause of aberrant migration of neural cells (neuronal ectopias) noted in brain at E11.5
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• at E10.5, epidermal and pial basement membranes are amorphously deposited or absent; in some areas the deposited material detaches from the surface of cells and forms irregular folds or is almost entirely absent
• in addition, deposited basement membrane-like matrices appear more irregular and less electron-dense
• however, basement membrane-like matrices are correctly deposited during early embryonic development, suggesting that secretion or deposition of laminins, nidogens or perlecan is normal
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