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Effects of clk-1 on Lifespan of Caenorhabditis elegans
Zhang Congjie, Wang Kejie, Liu Zhenya, Huang Jiatao, Zhou Huaibin, Lü Jianxin*
School of Laboratory Medicine and Life Sciences, Zhejiang Provincial Key Laboratory of Medical Genetics, Wenzhou Medical University, Wenzhou 325035, China
Abstract: clk-1 [clock (biological timing) abnormality-1] encodes an enzyme required in CoQ biosynthesis， a redox-active lipid which acts as an electron carrier in the electron transport chain of the mitochondria. And clk-1 is mutant is the first longevity of mitochondrial gene mutation. By studying the phenotypes and mitochondrial functions， we investigate that clk-1 mutant and clk-1 RNAi (RNA interference) had different influences on Lifespan. clk-1(qm30) mutant led to increased longevity， elevated the level of reactive oxygen species (ROS) in mitochondria and decreased the level of ROS in cytoplasm. clk-1(qm30) mutant had higher ATP content. While clk-1 RNAi led to shorten lifespan， decreased the level of mitochondrial ROS and elevated the level of cytoplasmic ROS. clk-1 RNAi had significant lower ATP content. ROS， as cell signaling molecule， has an important role in aging; ATP is a significant index of energy metabolism， and the higher level represents slow energy metabolism. We suppose the difference of lifespan may depend on the function of the mitochondrial and cytoplasmic ROS and energy metabolism.
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