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Role of gene SESN-1 in life extension of Caenorabditis elegans during food deprivation
Global Congress on Biochemistry, Glycomics & Amino Acids
December 08-09, 2016 San Antonio, USA

Andrey O. Zheltukhin, Peter M Chumakov

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia

Posters & Accepted Abstracts: Biochem Anal Biochem


It is known that the calories restriction prolongs lifespan to a wide range of living organisms, suppression of activity of TOR (a target of a rapamitsin) is the cornerstone of this phenomenon. A p53-regulated gene sesn-1 (Sestrin-1) is known as one of regulators of activity of TOR, and also as an antioxidant. In mammals sestrin- is a member of a family of three genes, and that complicate its studying. Therefore we chose a nematode Caenorabditis elegans, because it were only ortholog of the sestrin genes and even the complete food deprivation significantly extends nematode lifespan. In our work we showed that the gene sestrin is necessary for this phenomenon. Mean lifespan was compared for wild type and sesn-1-/- mutant with normal condition (food ad libitum) and with food deprivation, showed that sestrin-1-/-mutant lived average by 11,04% less than wt, in the absence of food the wild type lived longer by 40,23%, mutant lived longer only by 6,2%. To study mechanisms of the SESN effects we monitored the autophagy, and the phosphorylation of the TOR-kinase substrate protein rsp6. For this we used a genetic construct expressing the LC3 analog fused with GFP (LGG::GFP) that helps visualizing and counting autophagosomes. It revealed that food deprivation increased the autophagy by 416% for wild type and only by 61% for sesn-1-/-. Western blots have demonstrated the significant reduction of rps6 protein phosphorylation during starvation for wt but not for sesn-1-/-. It showed that sesn-1 is necessary for suppression of TOR that usually occurs at starvation. Conclusion: sestrin-1is required to extension of lifespan of nematodes at calorie restriction, sesn-1 inhibits TOR kinase affecting prs6 phosphorylation and inducing the autophagy. Acknowledgments: our research was supported by Russian Ministry of Education grant RFMEFI60714X0067.

Biography :

Andrey O. Zheltukhin yong rresearcher in Engelgardt Institute of Molecular Biology. The main directions of this theme, developed at the Institute of Molecular Biology, Russian Academy of Sciences.

Email: aozheltukhin@gmail.com