mortality/aging
• no viable homozygous mutant mice are observed in crosses between heterozygotes
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• homozygotes are present at expected Mendelian frequencies at E9.5 (24%) but die between E10.5 (14%) and E12.5 (0%), indicating mid-gestational lethality
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growth/size/body
• embryos exhibit delayed growth between E8.5 and E10.5
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• embryos are morphologically smaller than wild-type at E8.5-E10.5 but not at E7.5
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embryo
N |
• yolk sac formation is normal at E9.5
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• embryos exhibit delayed growth between E8.5 and E10.5
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• embryos are morphologically smaller than wild-type at E8.5-E10.5 but not at E7.5
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• absence of neural tube closure at E9.5-E10.5
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• major placental defects at E9.5-E11.5
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• Unr-rich NRs, a newly identified network of double-wall nuclear membrane invaginations that contain a cytoplasmic core related to the nucleoplasmic reticulum (NR), are absent in placental trophoblast giant cells (TGCs) at E10.5 and E11.5, unlike in wild-type controls
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• ~60-75% reduction in TGC number
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• marked atrophy of the spongiotrophoblast layer
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• marked atrophy of the labyrinth layer
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• abnormal placental development between E8.5 and E11.5
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cardiovascular system
• defect in ventricular trabeculation at E10.5
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• smaller than normal atrioventricular cushions at the atrioventricular canal at E10.5
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• heart maturation is delayed at E10.5
• however, heart is not critically abnormal
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nervous system
• absence of neural tube closure at E9.5-E10.5
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muscle
• defect in ventricular trabeculation at E10.5
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homeostasis/metabolism
• Unr-containing NRs, shown to contain high levels of poly(A) RNA and translation factors and to represent sites of active mRNA translation, are not formed in placental trophoblast giant cells (TGCs)
• nuclei of TGCs neither accumulate endoplasmic reticulum (ER) resident proteins nor translation factors in NR-like structures
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cellular
• Unr-containing NRs, shown to contain high levels of poly(A) RNA and translation factors and to represent sites of active mRNA translation, are not formed in placental trophoblast giant cells (TGCs)
• nuclei of TGCs neither accumulate endoplasmic reticulum (ER) resident proteins nor translation factors in NR-like structures
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