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Senoo-Matsuda, N, Hartman, PS, Akatsuka, A, Yoshimura, S and Ishii, N (2003) A complex II defect affects mitochondrial structure, leading to ced-3- and ced-4-dependent apoptosis and aging. J. Biol. Chem. 278:22031-6
The mev-1(kn1) mutation of Caenorhabditis elegans is in Cyt-1, which encodes a subunit of succinate-coenzyme Q oxidoreductase in the mitochondrial electron transport chain. Mutants are hypersensitive to oxidative stress and age precociously in part because of increased superoxide anion production. Here, we show that mev-1 mutants are defective in succinate-coenzyme Q oxidoreductase, possess ultrastructural mitochondrial abnormalities (especially in muscle cells), show a loss of membrane potential, have altered CED-9 and Cyt-1 protein levels under hyperoxia, and contain ced-3-and ced-4-dependent supernumerary apoptotic cells. These defects likely explain the failure of mev-1 to complete embryonic development under hyperoxia as well as its reduced life span.
Aging; Animals; Anoxia; Antibodies, Monoclonal/metabolism; Apoptosis; Apoptosis Regulatory Proteins; Blotting, Western; Caenorhabditis elegans; Caenorhabditis elegans Proteins/metabolism; Calcium-Binding Proteins/metabolism; Caspases/metabolism; Cytochromes/genetics; Cytochromes b; Immunohistochemistry; Membrane Potentials; Microscopy, Electron; Microscopy, Fluorescence; Mitochondria/metabolism; Models, Biological; Mutation; Oxygen/metabolism; Proto-Oncogene Proteins/metabolism; Proto-Oncogene Proteins c-bcl-2; Time Factors
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