AMPK-dependent and -independent coordination of mitochondrial function and muscle fiber type by FNIP1


Autoři: Liwei Xiao aff001;  Jing Liu aff001;  Zongchao Sun aff001;  Yujing Yin aff001;  Yan Mao aff001;  Dengqiu Xu aff001;  Lin Liu aff001;  Zhisheng Xu aff001;  Qiqi Guo aff001;  Chenyun Ding aff001;  Wanping Sun aff001;  Likun Yang aff001;  Zheng Zhou aff001;  Danxia Zhou aff001;  Tingting Fu aff001;  Wenjing Zhou aff002;  Yuangang Zhu aff002;  Xiao-Wei Chen aff002;  John Zhong Li aff003;  Shuai Chen aff004;  Xiaoduo Xie aff005;  Zhenji Gan aff001
Působiště autorů: MOE Key Laboratory of Model Animals for Disease Study, Department of Spine Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Chemistry and Biomedicine Innovation Center (ChemBIC), Model Animal Research... aff001;  Institute of Molecular Medicine, Peking University, Beijing, China aff002;  The Key Laboratory of Rare Metabolic Disease, Department of Biochemistry and Molecular Biology, The Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University, Nanjing, China aff003;  MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Nanjing University Medical School, Nanjing University, Nanjing, China aff004;  Department of Biochemistry, School of Medicine, Sun Yat-sen University, Shenzhen, China aff005
Vyšlo v časopise: AMPK-dependent and -independent coordination of mitochondrial function and muscle fiber type by FNIP1. PLoS Genet 17(3): e1009488. doi:10.1371/journal.pgen.1009488
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pgen.1009488

Souhrn

Mitochondria are essential for maintaining skeletal muscle metabolic homeostasis during adaptive response to a myriad of physiologic or pathophysiological stresses. The mechanisms by which mitochondrial function and contractile fiber type are concordantly regulated to ensure muscle function remain poorly understood. Evidence is emerging that the Folliculin interacting protein 1 (Fnip1) is involved in skeletal muscle fiber type specification, function, and disease. In this study, Fnip1 was specifically expressed in skeletal muscle in Fnip1-transgenic (Fnip1Tg) mice. Fnip1Tg mice were crossed with Fnip1-knockout (Fnip1KO) mice to generate Fnip1TgKO mice expressing Fnip1 only in skeletal muscle but not in other tissues. Our results indicate that, in addition to the known role in type I fiber program, FNIP1 exerts control upon muscle mitochondrial oxidative program through AMPK signaling. Indeed, basal levels of FNIP1 are sufficient to inhibit AMPK but not mTORC1 activity in skeletal muscle cells. Gain-of-function and loss-of-function strategies in mice, together with assessment of primary muscle cells, demonstrated that skeletal muscle mitochondrial program is suppressed via the inhibitory actions of FNIP1 on AMPK. Surprisingly, the FNIP1 actions on type I fiber program is independent of AMPK and its downstream PGC-1α. These studies provide a vital framework for understanding the intrinsic role of FNIP1 as a crucial factor in the concerted regulation of mitochondrial function and muscle fiber type that determine muscle fitness.

Klíčová slova:

Mitochondria – Mouse models – Muscle fibers – Muscle functions – Muscle proteins – Skeletal muscle fibers – Skeletal muscles – Slow-twitch muscle fibers


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