Abstract
In healthy cells, mitochondria continually divide and fuse to form a dynamic interconnecting network. The molecular machinery that mediates this organelle fission and fusion is necessary to maintain mitochondrial integrity, perhaps by facilitating DNA or protein quality control. This network disintegrates during apoptosis at the time of cytochrome c release and prior to caspase activation, yielding more numerous and smaller mitochondria. Recent work shows that proteins involved in mitochondrial fission and fusion also actively participate in apoptosis induction. This review will cover the recent advances and presents competing models on how the mitochondrial fission and fusion machinery may intersect apoptosis pathways.
MeSH terms
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Adaptor Proteins, Signal Transducing / physiology
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Animals
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Apoptosis / physiology*
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Apoptosis Regulatory Proteins / physiology
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Calcium-Calmodulin-Dependent Protein Kinases / physiology
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Cell Division / physiology
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Cell Fusion
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Cellular Senescence / physiology
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Cytochromes c / metabolism
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Death-Associated Protein Kinases
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Drosophila Proteins / physiology
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GTP Phosphohydrolases / physiology
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Humans
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Membrane Proteins / physiology
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Mitochondria / physiology*
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Mitochondrial Proteins / physiology
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Models, Biological
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Protein Processing, Post-Translational / physiology
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Proto-Oncogene Proteins c-bcl-2 / physiology
Substances
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Adaptor Proteins, Signal Transducing
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Apoptosis Regulatory Proteins
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Drosophila Proteins
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FIS1 protein, human
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Marf protein, Drosophila
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Membrane Proteins
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Mitochondrial Proteins
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Proto-Oncogene Proteins c-bcl-2
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SH3GLB1 protein, human
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Cytochromes c
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Death-Associated Protein Kinases
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Calcium-Calmodulin-Dependent Protein Kinases
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GTP Phosphohydrolases