Jonassen T, Proft M, Randez-Gil F, Schultz J R, Marbois B N, Entian K D, Clarke C F
Department of Chemistry and Biochemistry and the Molecular Biology Institute, University of California, Los Angeles, Los Angeles, California 90095, USA.
J Biol Chem. 1998 Feb 6;273(6):3351-7. doi: 10.1074/jbc.273.6.3351.
Mutations in the clk-1 gene result in slower development and increased life span in Caenorhabditis elegans. The Saccharomyces cerevisiae homologue COQ7/CAT5 is essential for several metabolic pathways including ubiquinone biosynthesis, respiration, and gluconeogenic gene activation. We show here that Coq7p/Cat5p is a mitochondrial inner membrane protein directly involved in ubiquinone biosynthesis, and that the defect in gluconeogenic gene activation in coq7/cat5 null mutants is a general consequence of a defect in respiration. These results obtained in the yeast model suggest that the effects on development and life span in C. elegans clk-1 mutants may relate to changes in the amount of ubiquinone, an essential electron transport component and a lipid soluble antioxidant.
clk-1基因的突变会导致秀丽隐杆线虫的发育迟缓以及寿命延长。酿酒酵母的同源物COQ7/CAT5对于包括泛醌生物合成、呼吸作用以及糖异生基因激活在内的多种代谢途径至关重要。我们在此表明，Coq7p/Cat5p是一种直接参与泛醌生物合成的线粒体内膜蛋白，并且coq7/cat5基因敲除突变体中糖异生基因激活的缺陷是呼吸作用缺陷的普遍结果。在酵母模型中获得的这些结果表明，秀丽隐杆线虫clk-1突变体对发育和寿命的影响可能与泛醌含量的变化有关，泛醌是一种必需的电子传递成分和脂溶性抗氧化剂。
