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Papers In Press, published online ahead of print April 12, 2004
Centro Andaluz de Biología del Desarrollo, Sevilla, Sevilla 41013
Corresponding Author: csanoca{at}dex.upo.es
Caenorhabditis elegans clk-1 mutants cannot produce coenzyme Q9 and instead accumulate demethoxy-Q9 (DMQ9). DMQ9 has been proposed to be responsible for the extended lifespan of clk-1 mutants, theoretically through its enhanced antioxidant properties and its decreased function in respiratory chain electron transport. In the present study we assess the functional roles of DMQ6 in the yeast Saccharomyces cerevisiae. Three mutations designed to mirror the clk-1 mutations of C. elegans were introduced into COQ7, the yeast homologue of clk-1: E233K, predicted to disrupt the diiron carboxylate site considered essential for hydroxylase activity; L237Stop, a deletion of 36 amino acid residues from the carboxyl terminus; and P175Stop, a deletion of the carboxyl-terminal half of Coq7p. Growth on glycerol, quinone content, respiratory function, and response to oxidative stress were analyzed in each of the coq7 mutant strains. Yeast strains lacking Q6 and producing solely DMQ6 were respiratory deficient and unable to support either NADH-cytochrome c reductase or succinate-cytochrome c reductase activities. DMQ6 failed to protect cells against oxidative stress generated by H2O2 or linolenic acid. Thus, in the yeast model system, DMQ does not support respiratory activity and fails to act as an effective antioxidant. These results suggest that the life span extension observed in the C. elegans clk-1 mutants cannot be attributed to the presence of DMQ per se.
J. Biol. Chem, 10.1074/jbc.M400001200
Submitted on January 1, 2004
Revised on April 12, 2004
Accepted on April 12, 2004
Demethoxy-Q, an intermediate of coenzyme Q biosynthesis, fails to support respiration in saccharomyces cerevisiae and lacks antioxidant activity
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