作者
Sergio Padilla, Tanya Jonassen, María A Jiménez-Hidalgo, Daniel José M Fernández-Ayala, Guillermo López-Lluch, Beth Marbois, Plácido Navas, Catherine F Clarke, Carlos Santos-Ocana
发表日期
2004/6/18
期刊
Journal of Biological Chemistry
卷号
279
期号
25
页码范围
25995-26004
出版商
Elsevier
简介
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 di-iron 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 …
引用总数
学术搜索中的文章
S Padilla, T Jonassen, MA Jiménez-Hidalgo… - Journal of Biological Chemistry, 2004