Phenotypes associated with this allele
Allelic Composition |
Zfpm2tm1.1Esv/Zfpm2tm1.1Esv
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Genetic Background |
involves: 129S1/SvImJ * 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6 |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zfpm2tm1.1Esv mutation
(0 available);
any
Zfpm2 mutation
(47 available)
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cardiovascular system
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• at birth, mutant hearts display a thin myocardial compact zone
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• atrial septal defects are present at P0
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• ventricular septal defects are present at P0
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• at P0, echocardiography revealed a reduction in systolic function as determined by left ventricular fractional shortening
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• at P0, echocardiographic M-mode tracings revealed a significant increase in left ventricular end systolic dimension (LVESD) relative to control mice
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muscle
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• at birth, mutant hearts display a thin myocardial compact zone
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• at P0, echocardiography revealed a reduction in systolic function as determined by left ventricular fractional shortening
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Allelic Composition |
Zfpm2tm1.1Esv/Zfpm2+
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Genetic Background |
involves: 129S1/SvImJ * 129S4/SvJae * 129S6/SvEvTac |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Zfpm2tm1.1Esv mutation
(0 available);
any
Zfpm2 mutation
(47 available)
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normal phenotype
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• heterozygotes are viable and fertile, display no grossly overt malformations, and have a normal lifespan
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn1atm1Tyj mutation
(3 available);
any
Cdkn1a mutation
(60 available)
Zfpm2tm1.1Esv mutation
(0 available);
any
Zfpm2 mutation
(47 available)
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muscle
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• at birth, double homozygotes display a significantly thicker myocardial compact zone than single Zfpm2tm1.1Esv homozygotes; however, left ventricular wall thickness is still not completely normal
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mortality/aging
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• double homozygotes die by P14, possibly due to septal defects
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cardiovascular system
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• at birth, double homozygotes display a significantly thicker myocardial compact zone than single Zfpm2tm1.1Esv homozygotes; however, left ventricular wall thickness is still not completely normal
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• atrial septal defects are still present at P0
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• ventricular septal defects are still present at P0
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• at birth, double homozygotes show only a modest 26.8 +/- 3.2% rescue of left ventricular wall thickness relative to wild-type controls
• however, left ventricular fractional shortening is preserved, indicating that increased wall thickness improves left ventricular function
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• at P0, echocardiographic M-mode tracings revealed a slight increase in left ventricular end diastolic dimension (LVEDD) relative to wild-type controls, suggesting that mutant hearts are starting to dilate and fail
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