Analysis Tools
mortality/aging
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• embryos die around E9.5 following developmental arrest and severe cardiovascular malformations
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growth/size/body
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• all embryos show developmental delay at E9.5
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• embryo size is decreased at E9.5-E11.5
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• at E9.5, embryos show a smaller cephalic region with poorly defined subdivisions of the primitive brain vesicles
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embryo
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• yolk sac vessel development is arrested at the honeycomb-shaped capillary plexus stage
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• the yolk sac is systematically devoid of well-developed vessels
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• 19% of embryos with pronounced stunted growth or developmental delay show incomplete turning at E9.5; after removing annexes, these embryos appear as erected E8.5 embryos
• however, remaining 81% embryos have completed their turning by E9.5
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• all embryos show developmental delay at E9.5
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• embryos appear very abnormal at E10.5 and E11.5; in some cases, first signs of resorption include a truncated caudal part and a collapsed heart
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• at E10.5 and E11.5, embryos show absence of well-defined branchial arches
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• embryo size is decreased at E9.5-E11.5
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• at E10.5 and E11.5, embryos show absence of protruding limb buds
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• in many cases, the anterior neuropore remains open at E9.5
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• embryos that have completed their turning exhibit fewer pairs of somites than expected, enabling to classify them as E9.0 to E9.25 embryos
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• no red blood cells are visible
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cardiovascular system
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• erythrocytes are rarely observed in the head vessels
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• myocardium shows reduced thickness
• however, cardiac jelly is present between the endocardium and the myocardium and myocardial cell differentiation is normal
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• E9.5 embryos show abnormal cardiovascular development associated with absence of blood flow and pericardial edema despite cardiac beating, suggesting insufficient contractile force of the myocardium
• although red blood cells are present, they accumulate in the venous network and are rarely observed in the dorsal aortae or in the cardiac chamber
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• embryos exhibit poor embryonic and extra-embryonic vascular development, with thin and short peripheral vessels and no visible vessels in the yolk sac
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• intersomitic vascular ramifications are poorly developed
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• caudal expansion of the posterior cardinal vein is poorly developed
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• yolk sac vessel development is arrested at the honeycomb-shaped capillary plexus stage
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• the yolk sac is systematically devoid of well-developed vessels
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• cardiac development is arrested at ~E8.5 concomitant with a precocious termination of embryo development
• even in the most E9.5 advanced embryos, the beating heart is not compartmentalized; in most cases, it appears in a U-shaped tubular form that contains no erythrocytes
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• in most cases, the heart remains at the heart tube stage, a feature of the late E8.5 stage
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• at E10.5 and E11.5, erythrocytes are very often found sedimenting in the pericardial cavity
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• at E9.5-E11.5, most embryos exhibit pericardial edema
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cellular
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• at E9.5, many mitochondria appear dilated and are abnormally compartmentalized in the myocardium, endocardium, foregut, and branchial arch
• in the myocardium, 37% of mitochondria show compartmentalization versus 12% in wild-type embryos
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• at E9.5, most mitochondria exhibit abnormal cristae shape and organization, leading to either to vesicle-like cristae or to compartmentalization of mitochondria
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• at E9.5, both phosphorylating and non-phosphorylating respirations are significantly decreased, with a stronger impact on phosphorylating respiration, leading to a marked reduction in the respiratory control ratio (i.e., ratio of phosphorylating to non-phosphorylating oxidation rate)
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• at E9.5, respiratory chain efficiency and the coupling between the respiratory chain and the ATP synthase is affected
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• although cardiolipin relative content is normal in E9.5 embryos, in-depth analysis showed abnormal cardiolipin profiles with many mono- or di-oxidized cardiolipin species, yielding a total of 16% of oxidized cardiolipins versus 0.7% in wild-type embryos
• however, cardiolipin oxidation triggers no major antioxidative defense, as determined by mRNA expression levels of genes involved in oxidative stress response (Sod2, Gpx1 and Cat)
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homeostasis/metabolism
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• at E10.5 and E11.5, erythrocytes are very often found sedimenting in the pericardial cavity
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• at E9.5-E11.5, most embryos exhibit pericardial edema
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• although cardiolipin relative content is normal in E9.5 embryos, in-depth analysis showed abnormal cardiolipin profiles with many mono- or di-oxidized cardiolipin species, yielding a total of 16% of oxidized cardiolipins versus 0.7% in wild-type embryos
• however, cardiolipin oxidation triggers no major antioxidative defense, as determined by mRNA expression levels of genes involved in oxidative stress response (Sod2, Gpx1 and Cat)
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• E9.5 embryos show a significant higher relative phosphatidylserine content (expressed as a % of total phospholipid content) than wild-type embryos
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limbs/digits/tail
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• at E10.5 and E11.5, embryos show absence of protruding limb buds
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• at E9.5-E11.5, some embryos exhibit a poorly defined tail
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muscle
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• myocardium shows reduced thickness
• however, cardiac jelly is present between the endocardium and the myocardium and myocardial cell differentiation is normal
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nervous system
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• in many cases, the anterior neuropore remains open at E9.5
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• at E10.5 and E11.5, embryos show absence of salient cephalic vesicles
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craniofacial
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• at E10.5 and E11.5, embryos show absence of well-defined branchial arches
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vision/eye
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• at E10.5 and E11.5, embryos show absence of pigmented optic vesicles
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