IF1, a natural inhibitor of mitochondrial ATP synthase,is not essential for the normal growth and breeding of mice |
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Authors: | Junji Nakamura Makoto Fujikawa Masasuke Yoshida |
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Affiliation: | *Department of Molecular Bioscience, Kyoto Sangyo University, Kamigamo-Motoyama, Kyoto 603-8555, Japan;†International Cooperative Research Project (ICORP) ATP-Synthesis Regulation Project, Japan Science and Technology Agency (JST), 2-3-6 Aomi, Tokyo 135-0064, Japan;‡Department of Biochemistry, Tokyo University of Science, 2641 Yamazaki, Noda 278-8510, Japan |
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Abstract: | IF1 is an endogenous inhibitor protein of mitochondrial ATP synthase. It is evolutionarily conserved throughout all eukaryotes and it has been proposed to play crucial roles in prevention of the wasteful reverse reaction of ATP synthase, in the metabolic shift from oxidative phosphorylation to glycolysis, in the suppression of ROS (reactive oxygen species) generation, in mitochondria morphology and in haem biosynthesis in mitochondria, which leads to anaemia. Here, we report the phenotype of a mouse strain in which IF1 gene was destroyed. Unexpectedly, individuals of this IF1-KO (knockout) mouse strain grew and bred without defect. The general behaviours, blood test results and responses to starvation of the IF1-KO mice were apparently normal. There were no abnormalities in the tissue anatomy or the autophagy. Mitochondria of the IF1-KO mice were normal in morphology, in the content of ATP synthase molecules and in ATP synthesis activity. Thus, IF1 is not an essential protein for mice despite its ubiquitous presence in eukaryotes. |
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Keywords: | ATP synthesis FoF1 knockout mouse |
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