Analysis Tools
normal phenotype
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• mice are viable, fertile and show no obvious phenotypic abnormalities
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Allele Symbol Allele Name Allele ID |
Casz1tm1.1Flc targeted mutation 1.1, Frank Conlon MGI:5638931 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice are viable, fertile and show no obvious phenotypic abnormalities
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• no viable embryos are identified after E14.5
• however, embryos appear grossly normal at E12.5
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• severe thinning of the myocardium by E12.5
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• abnormal heart development between E10.5 and E12.5
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• at E12.5, the number of tropomyosin (TMY)-positive cardiomyocytes is significantly reduced in the ventricles
• however, no increase in programmed cell death is observed and actin filaments are intact
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• heart fails to form an apex for either the left or the right ventricle
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• enlarged right atrium at E12.5; more pronounced at E13.5
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• ballooning of the right atria by E13.5, indicating blood pooling in the right ventricle
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• misshapen heart at E13.5
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• severe cardiac hypoplasia by E13.5
• at E12.5, cardiac hypoplasia is specific to cardiomyocytes and does not affect the epicardium or endothelial cells
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• narrower ventricular lumens by E13.5
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• decreased trabeculation at E12.5
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• underdeveloped interventricular septum at E12.5
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• membranous ventricular septal defects by E13.5
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• malformed left ventricle at E12.5; more pronounced at E13.5
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• thinning of the ventricular walls starting at E12.5
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• inflated pericardial sacs at E13.5
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• severe blood hemorrhaging at E13.5
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• decreased blood flow throughout the vasculature by E13.5
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• at E12.5, the G1-to-S phase progression of cardiomyocytes is impaired, as shown by a prolonged or arrested G1 phase, a reduction in DNA synthesis, an increase in phospho-RB, and a decrease in the cardiac mitotic index
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• cardiomyocyte proliferation is significantly reduced in E12.5 ventricles, as shown by EdU incorporation
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• cardiomyocyte proliferation is significantly reduced in E12.5 ventricles, as shown by EdU incorporation
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• at E12.5, cell cycle profiling of cardiac nuclei revealed a significant increase of cells in G1 phase and a simultaneous decrease of cells in S phase, with no alteration in the % of cells in G2 phase
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• cardiomyocyte mitotic index is significantly reduced in E12.5 ventricles, as shown by phospho-histone H3 staining
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• decreased trabeculation at E12.5
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• severe thinning of the myocardium by E12.5
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• cardiomyocyte proliferation is significantly reduced in E12.5 ventricles, as shown by EdU incorporation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• embryos are viable and indistinguishable from controls at least until E14.5; however, no mice are recovered postnatally
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• misshapen heart at E14.5
• however, no ventricular septal defects are detected at E14.5
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• right ventricular wall thickness is significantly reduced at E14.5
• however, left ventricular wall thickness is normal
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• right ventricular hypoplasia at E14.5
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• at E12.5, cardiomyocyte mitotic index is significantly reduced in the right ventricles (but not in the left ventricles), as shown by phospho-histone H3 staining
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• embryos do not survive past E14.5
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• at E12.5, embryos show a cardiac phenotype indistinguishable from that of embryos homozygous for Casz1tm1.1Flc and heterozygous for Nkx2-5tm1(cre)Rjs
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• at E12.5
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• severe cardiac hypoplasia at E12.5
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• at E12.5
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 05/07/2024 MGI 6.23 |
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