Lee, Byung CheonLee, Hae MinKim, SorahAvanesov, Andrei S.Lee, AroChun, Bok-HwanVorbruggen, GerdGladyshev, Vadim2018-03-202018Lee, Byung Cheon, Hae Min Lee, Sorah Kim, Andrei S. Avanesov, Aro Lee, Bok-Hwan Chun, Gerd Vorbruggen, and Vadim N. Gladyshev. 2018. “Expression of the methionine sulfoxide reductase lost during evolution extends Drosophila lifespan in a methionine-dependent manner.” Scientific Reports 8 (1): 1010. doi:10.1038/s41598-017-15090-5. http://dx.doi.org/10.1038/s41598-017-15090-5.http://nrs.harvard.edu/urn-3:HUL.InstRepos:35014374Accumulation of oxidized amino acids, including methionine, has been implicated in aging. The ability to reduce one of the products of methionine oxidation, free methionine-R-sulfoxide (Met-R-SO), is widespread in microorganisms, but during evolution this function, conferred by the enzyme fRMsr, was lost in metazoa. We examined whether restoration of the fRMsr function in an animal can alleviate the consequences of methionine oxidation. Ectopic expression of yeast fRMsr supported the ability of Drosophila to catalyze free Met-R-SO reduction without affecting fecundity, food consumption, and response to starvation. fRMsr expression also increased resistance to oxidative stress. Moreover, it extended lifespan of flies in a methionine-dependent manner. Thus, expression of an oxidoreductase lost during evolution can enhance metabolic and redox functions and lead to an increase in lifespan in an animal model. More broadly, our study exposes the potential of a combination of genetic and nutritional strategies in lifespan control.en-USExpression of the methionine sulfoxide reductase lost during evolution extends Drosophila lifespan in a methionine-dependent mannerJournal Article2018-03-2010.1038/s41598-017-15090-5