Analysis Tools
cellular
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• mitochondrial fragmentation in mouse embryonic fibroblasts treated with cre-expressing adenovirus
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Allele Symbol Allele Name Allele ID |
Mfn2tm1.1Mzhe targeted mutation 1.1, Ming Zheng MGI:5445195 |
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| Summary |
2 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mitochondrial fragmentation in mouse embryonic fibroblasts treated with cre-expressing adenovirus
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Autophagosome accumulation in Mfn2tm1.1Mzhe/Mfn2tm1.1Mzhe Myl2tm1(cre)Krc/Myl2+ hearts
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• cardiomyocytes exhibit increased numbers of large mitochondria and average size of mitochondrial area compared with cells from control mice
• cardiomyocytes contain large numbers of double and multimembrane autophagosome-like vacuolar structures and increased autophagic activity compared with cells from control mice
• cardiomyocytes exhibit impaired autophagosome-lysosome fusion compared with cells from control mice
• cardiomyocytes exhibit endoplasmic reticulum stress unlike cells from control mice
• however, cardiomyocytes exhibit normal mitochondrial mass and autophagosome formation
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• beginning at 17 months of age
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• at 12 months following ischemia-reperfusion stress
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• following ischemia-reperfusion stress, cardiomyocytes from 6 month old mice exhibit a greater loss of mitochondrial membrane potential compared with cells from control mice
• however, mitochondrial membrane potential is normal at 4 months following ischemia-reperfusion stress
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• following ischemia-reperfusion stress, cardiomyocytes from 6 month old mice exhibit a greater loss of mitochondrial membrane potential compared with cells from control mice
• worse at 12 months of age with increased cardiomyocytes apoptosis
• however, mitochondrial membrane potential is normal at 4 months following ischemia-reperfusion stress
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• at 12 months following ischemia-reperfusion stress
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• cardiomyocytes exhibit increased numbers of large mitochondria and average size of mitochondrial area compared with control mice
• however, mitochondrial mass is normal
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• cardiomyocytes contain large numbers of double and multi-membrane autophagosome-like vacuolar structures and increased autophagic activity compared with cells from control mice
• cardiomyocytes exhibit impaired autophagosome-lysosome fusion compared with cells from control mice
• however, autophagosome formation is normal
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• decreased respiratory control ration in the cardiomyocytes
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• in the heart
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• cardiomyocytes exhibit increased numbers of large mitochondria and average size of mitochondrial area compared with cells from control mice
• cardiomyocytes contain large numbers of double and multimembrane autophagosome-like vacuolar structures and increased autophagic activity compared with cells from control mice
• cardiomyocytes exhibit impaired autophagosome-lysosome fusion compared with cells from control mice
• cardiomyocytes exhibit endoplasmic reticulum stress unlike cells from control mice
• however, cardiomyocytes exhibit normal mitochondrial mass and autophagosome formation
|
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• beginning at 17 months of age
|
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• following ischemia-reperfusion stress, cardiomyocytes from 6 month old mice exhibit a greater loss of mitochondrial membrane potential compared with cells from control mice
• worse at 12 months of age with increased cardiomyocytes apoptosis
• however, mitochondrial membrane potential is normal at 4 months following ischemia-reperfusion stress
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• cardiomyocytes contain large numbers of double and multi-membrane autophagosome-like vacuolar structures and increased autophagic activity compared with cells from control mice
• cardiomyocytes exhibit impaired autophagosome-lysosome fusion compared with cells from control mice
• however, autophagosome formation is normal
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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 04/23/2024 MGI 6.23 |
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