Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Nrastm1Rak mutation
(1 available);
any
Nras mutation
(44 available)
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normal phenotype
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• viable and fertile; no gross morphological or histological abnormalities, or defects in peripheral blood cell populations were detected in homozygous mice
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normal phenotype
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• mice grew normally, were fertile and did not exhibit any obvious phenotype; however, fewer than the expected number of adult compound homozygous mice were obtained in crosses
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mortality/aging
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• ~40% of mutant embryos are found dead at E9.5
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mortality/aging
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• ~30% of these mutants die perinatally
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• a few mutant embryos survive up to P2, but are subsequently neglected by their mothers and die shortly thereafter
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• ~70% of these mutants die between E10.0 and E12.0
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cardiovascular system
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• at E10.5, mutant embryos display dilated pericardial sacs
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• at E10.5, mutant embryos exhibit a dilated heart
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embryo
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• by E10.5, cell death extends throughout the entire embryo
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• at E10.5, mutant embryos appear to have arrested at ~E9.5
• ~30% of abnormal mutant embryos survive beyond this early developmental block but are readily identifiable up until the final stages of gestation
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• by E10.5, 65% of viable mutant embryos appear grossly abnormal
• starting at E9.5, ~50% of mutants are delayed by 0.5-1.0 developmental days, but never show the non-coordinate delay observed in late Krastm1Tyj embryos
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• at E10.5, mutant embryos display a near or complete absence of blood islands in yolk sacs
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• at E10.5, mutant yolk sacs appear rough and wrinkled
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• at E10.5, mutant embryos exhibit significantly reduced numbers of circulating primitive erythrocytes in either the yolk sac or the embryo
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homeostasis/metabolism
cellular
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• at E9.5, mutant embryos display prominent cell death in the forebrain, and to a lesser extent along the neural axis
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• by E10.5, cell death extends throughout the entire embryo
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hematopoietic system
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• at E10.5, mutant embryos exhibit significantly reduced numbers of circulating primitive erythrocytes in either the yolk sac or the embryo
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• at E15.5-16.5, mutant fetal livers display a significantly reduced ratio in the number of erythroblasts to hepatocytes
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• at E15.5, viable mutant embryos are developmentally delayed and severely anemic
• anemia appears to be attributable to inadequate, but apparently normal, production of definitive erythrocytes and may reflect a defect in the survival or differentiation of either the erythroblasts or a more primitive progenitor cells
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vision/eye
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• 22% of E13.5-18.5 mutant embryos display an asymmetrical pattern in eye development, involving only the right eye
• either the right eye is significantly smaller than its wild-type counterpart or the pigment of the eye is overgrown
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limbs/digits/tail
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• 20% of E13.5-18.5 mutant embryos exhibit severe shortening of the tail
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liver/biliary system
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• by 16.5, a high % of mutant hepatocytes appear extremely vacuolated in the absence of increased cell death
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growth/size/body
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• by E10.5, 65% of viable mutant embryos appear grossly abnormal
• starting at E9.5, ~50% of mutants are delayed by 0.5-1.0 developmental days, but never show the non-coordinate delay observed in late Krastm1Tyj embryos
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integument
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• at E10.5, mutant embryos are significantly paler than wild-type embryos
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mortality/aging
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• double homozygous mutant blastocyst stage embryos are recovered at approximately the expected frequency of 6%
• no viable double mutant embryos are recovered at E9.5
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Analysis Tools
