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HDAC6 regulates lipid droplet turnover in response to nutrient deprivation via p62-mediated selective autophagy.

Authors
  • Yan, Yan1
  • Wang, Hao2
  • Wei, Chuanxian1
  • Xiang, Yuanhang3
  • Liang, Xuehong3
  • Phang, Chung-Weng4
  • Jiao, Renjie5
  • 1 Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, China; State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, The Chinese Academy of Sciences, Beijing, 100101, China. , (China)
  • 2 Department of Chemistry and Biology, National University of Defense Technology, Changsha, 410072, China. , (China)
  • 3 State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, The Chinese Academy of Sciences, Beijing, 100101, China. , (China)
  • 4 Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, China. , (China)
  • 5 Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China; The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, China; State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, The Chinese Academy of Sciences, Beijing, 100101, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Journal of Genetics and Genomics
Publisher
Elsevier
Publication Date
Apr 20, 2019
Volume
46
Issue
4
Pages
221–229
Identifiers
DOI: 10.1016/j.jgg.2019.03.008
PMID: 31078436
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Autophagy has been evolved as one of the adaptive cellular processes in response to stresses such as nutrient deprivation. Various cellular cargos such as damaged organelles and protein aggregates can be selectively degraded through autophagy. Recently, the lipid storage organelle, lipid droplet (LD), has been reported to be the cargo of starvation-induced autophagy. However, it remains largely unknown how the autophagy machinery recognizes the LDs and whether it can selectively degrade LDs. In this study, we show that Drosophila histone deacetylase 6 (dHDAC6), a key regulator of selective autophagy, is required for the LD turnover in the hepatocyte-like oenocytes in response to starvation. HDAC6 regulates LD turnover via p62/SQSTM1 (sequestosome 1)-mediated aggresome formation, suggesting that the selective autophagy machinery is required for LD recognition and degradation. Furthermore, our results show that the loss of dHDAC6 causes steatosis in response to starvation. Our findings suggest that there is a potential link between selective autophagy and susceptible predisposition to lipid metabolism associated diseases in stress conditions. Copyright © 2019 Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, and Genetics Society of China. Published by Elsevier Ltd. All rights reserved.

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