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ATP5B regulates mitochondrial fission and fusion in mammalian cells

Animal Cells and Systems 2016년 20권 3호 p.157 ~ 164
서혜민, 이익수, 정학석, 배규운, 장민선, 송은숙, 김민중,
소속 상세정보
서혜민 ( Seo Hye-Min ) - Sookmyung Women’s University Department of Biological Sciences
이익수 ( Lee Ick-Soo ) - Dankook University College of Medicine
정학석 ( Chung Hak-Suk ) - Korea Institute of Science and Technology Biomedical Research Institute Center for Theragnosis
배규운 ( Bae Gyu-Un ) - Sookmyung Women’s University College of Pharmacy
장민선 ( Chang Min-Sun ) - Sookmyung Women’s University Department of Biological Sciences
송은숙 ( Song Eun-Sook ) - Sookmyung Women’s University Department of Biological Sciences
김민중 ( Kim Min-Jung ) - Sookmyung Women’s University Department of Biological Science

Abstract


Mitochondria are essential organelles that produce ATP and regulate cell growth, proliferation, and cell death. To maintain homeostasis, fusion and fission of mitochondria must be strictly regulated. Even though oligomerization of ATP synthase could affect the mitochondrial morphology, the exact mechanism is not clear. We confirmed that structure and function of ATP5B, which is a major component of the catalytic center of ATP synthase complexes, are closely connected to the mitochondrial morphology. ATP5B itself can enhance elongation of mitochondria. Moreover, mutations of the threonine residue at β-barrel domain, and the serine residue at nucleotide-binding domain of ATP5B, produce the opposite effect on the fission and fusion of mitochondrial networks. Here, we demonstrate that ATP5B is clearly involved in the mechanism of regulation for mitochondrial fusion and fission in mammalian cells.

키워드

Mitochondria; ATP5B; fission; fusion

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