Investigation on the functions of mitochondrial methionyl-tRNA formyltransferase(MTFMT) in anti-bacterial responses Jung-Hwa Seo1, Areum Jo1, and Joo-Yeon Yoo1* 1Department of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Republic of Korea
Mitochondria are evolved from primitive aerobic bacteria as described in “Endosymbiosis” theory, therefore protein translational system which occurs within mitochondria chooses a way of prokaryotes, meaning that translation initiates with N-formyl methionine, not methionine. Mitochondrial methionyl-tRNA formyltransferase(MTFMT) is a key enzyme by which tRNAfMet is provided with formyl group donated from N10-formyltetrahydrofolate. Recently, it has been reported that its mutation associates with Leigh syndrome by causing impaired mitochondrial translation. Here we report an observation that mitochondrial dysfunction regulates cellular immune responses especially against S.flexneri infection. MTFMT knock-down induces depolarization of mitochondrial membrane potential and decreases mitochondrial activity under infected condition. In addition, knock-down of MTFMT significantly restricts intracellular bacterial replication, which implies that particular type of mitochondrial dysfunction such as impaired translation or loss of mitochondrial membrane potential which is caused by MTFMT knock-down affects cellular anti-bacterial responses.
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