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SENP1-Sirt3 Signaling Controls Mitochondrial Protein Acetylation and Metabolism

文献类型：期刊论文

作者Wang, Tianshi2,3; Cao, Ying2,3; Zheng, Quan2,3; Tu, Jun2,3; Zhou, Wei2,3; He, Jianli2,3; Zhong, Jie2; Chen, Yalan2,3; Cai, Rong2,3; Zuo, Yong2,3
刊名MOLECULAR CELL
出版日期2019
卷号75期号:4页码:823-+
ISSN号1097-2765
DOI10.1016/j.molcel.2019.06.008
文献子类Article
英文摘要Sirt3, as a major mitochondrial nicotinamide adenine dinucleotide (NAD)-dependent deacetylase, is required for mitochondrial metabolic adaption to various stresses. However, how to regulate Sirt3 activity responding to metabolic stress remains largely unknown. Here, we report Sirt3 as a SUMOylated protein in mitochondria. SUMOylation suppresses Sirt3 catalytic activity. SUMOylation-deficient Sirt3 shows elevated deacetylation on mitochondrial proteins and increased fatty acid oxidation. During fasting, SUMO-specific protease SENP1 is accumulated in mitochondria and quickly de-SUMOylates and activates Sirt3. SENP1 deficiency results in hyper-SUMOylation of Sirt3 and hyper-acetylation of mitochondrial proteins, which reduces mitochondrial metabolic adaption responding to fasting. Furthermore, we find that fasting induces SENP1 translocation into mitochondria to activate Sirt3. The studies on mice show that Sirt3 SUMOylation mutation reduces fat mass and antagonizes high-fat diet (HFD)-induced obesity via increasing oxidative phosphorylation and energy expenditure. Our results reveal that SENP1-Sirt3 signaling modulates Sirt3 activation and mitochondrial metabolism during metabolic stress.
学科主题Biochemistry & Molecular Biology ; Cell Biology
WOS关键词FATTY-ACID OXIDATION ; SUMO-SPECIFIC PROTEASE-1 ; CALORIE RESTRICTION ; CRYSTAL-STRUCTURES ; TUMOR-SUPPRESSOR ; SIRT3 ; DEHYDROGENASE ; DEACETYLATION ; HYPERACETYLATION ; TRANSCRIPTION
语种英语
WOS记录号WOS:000482212200015
出版者CELL PRESS
版本出版稿
源URL[http://202.127.25.144/handle/331004/1313]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Jiao Tong Univ, Sch Med, Inst Immunol, Shanghai 200025, Peoples R China;
2.Shanghai Jiao Tong Univ, Dept Biochem & Mol Cell Biol, Shanghai Key Lab Tumor Microenvironm & Inflammat, Sch Med, Shanghai 200025, Peoples R China;
3.Shanghai Jiao Tong Univ, Sch Med, Renji Hosp, State Key Lab Oncogenes & Related Genes, Shanghai 200127, Peoples R China;
4.Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Endocrinol & Metab, Shanghai 200025, Peoples R China;
5.Shanghai Tongren Hosp, Fac Basic Med, Hongqiao Int Inst Med, Shanghai 200050, Peoples R China;
6.East China Normal Univ, Inst Biomed Sci, Shanghai 200241, Peoples R China;
7.Shanghai Jiao Tong Univ, Sch Med, Shanghai Gen Hosp, Inst Translat Med, Shanghai 201620, Peoples R China;
8.Shanghai Jiao Tong Univ, Sch Med, Chinese Acad Sci, Inst Hlth Sci, Shanghai 200031, Peoples R China,
推荐引用方式
GB/T 7714		 Wang, Tianshi,Cao, Ying,Zheng, Quan,et al. SENP1-Sirt3 Signaling Controls Mitochondrial Protein Acetylation and Metabolism[J]. MOLECULAR CELL,2019,75(4):823-+.
APA Wang, Tianshi.,Cao, Ying.,Zheng, Quan.,Tu, Jun.,Zhou, Wei.,...&,.(2019).SENP1-Sirt3 Signaling Controls Mitochondrial Protein Acetylation and Metabolism.MOLECULAR CELL,75(4),823-+.
MLA Wang, Tianshi,et al."SENP1-Sirt3 Signaling Controls Mitochondrial Protein Acetylation and Metabolism".MOLECULAR CELL 75.4(2019):823-+.

入库方式： OAI收割

来源：上海营养与健康研究所

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