Translocation of mitochondrial aspartate aminotransferase through mitochondrial inner membrane. A cross-linking study with dimethyladipimidate.
Mitoplasts isolated from rat liver mitochondria were treated with dimethyladipimidate, a bifunctional alkylating agent. This agent causes, concurrently with modification of amino groups, loss of osmotic response. It was found that after cross-linking, the movement effector, succinate, was unable to induce the aspartate aminotransferase release from mitoplasts. In contrast, dimethyladipimidate-treated mitoplasts were still able to internalize 125I-labeled aspartate aminotransferase upon removal of exogenous succinate. The possible involvement of membrane asymmetry in the mechanism of translocation of porteins through the inner mitochondrial membrane is discussed.
D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism*; D003432:Cross-Linking Reagents; D004119:Dimethyl Adipimidate; D007425:Intracellular Membranes / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000201:enzymology*; D051381:Rats; D013386:Succinates / Q000378:metabolism; D013395:Sucrose / Q000378:metabolism
D003432:Cross-Linking Reagents; D013386:Succinates; D004119:Dimethyl Adipimidate; D013395:Sucrose; D001219:Aspartate Aminotransferases