C.elegans中clk-1基因对寿命的影响

Effects of clk-1 on Lifespan of Caenorhabditis elegans

clk-1[clock(biological timing)abnormality-1]是泛醌合成所必需的,参与电子传递过程,从而影响线粒体呼吸功能,其突变是已发现的第一个寿命延长的线粒体基因突变。该文通过对线虫表型、线粒体功能的相关检测来研究clk-1突变和clk-1 RNAi(RNA interference)对线虫寿命的影响。结果表明,clk-1突变线虫MQ130寿命延长,线粒体中活性氧类(reactive oxygen species,ROS)水平升高而胞质中ROS水平下降,总ATP含量升高;clk-1 RNAi线虫寿命缩短,线粒体中ROS水平下降而胞质中ROS水平升高,总ATP含量下降。ROS作为细胞的一种信号分子,与线虫的衰老密切相关;ATP是能量代谢的一个重要指标,其含量的升高代表着能量代谢缓慢。由此可见,clk-1突变线虫和clk-1RNAi线虫寿命的差异可能与线粒体和胞质中ROS的不同功能以及能量代谢速率的不同有关。

clk-1 [clock（biological timing） abnormality-1] encodes an enzyme required in Co Q 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.