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ATP5B regulates mitochondrial fission and fusion in mammalian cellsopen access

Authors
Seo, HyeminLee, IcksooChung, Hak SukBae, Gyu-UnChang, MinsunSong, EunsookKim, Min Jung
Issue Date
Jun-2016
Publisher
TAYLOR & FRANCIS LTD
Keywords
Mitochondria; ATP5B; fission; fusion
Citation
ANIMAL CELLS AND SYSTEMS, v.20, no.3, pp 157 - 164
Pages
8
Journal Title
ANIMAL CELLS AND SYSTEMS
Volume
20
Number
3
Start Page
157
End Page
164
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/9786
DOI
10.1080/19768354.2016.1188855
ISSN
1976-8354
2151-2485
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 -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.
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이과대학 (생명시스템학부)
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