Hao Wang
Chuanxian Wei
Yuanhang Xiang
Xuehong Liang
Chung-Weng Phang
Renjie Jiao
aSino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China
bThe Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510260, China
cState Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, The Chinese Academy of Sciences, Beijing, 100101, China
dDepartment of Chemistry and Biology, National University of Defense Technology, Changsha, 410072, China
More InformationCorresponding author: E-mail address: rjiao@sun5.ibp.ac.cn (Renjie Jiao)
Received Date: 2018-06-11
Accepted Date:2019-03-12
Rev Recd Date:2019-03-03
Available Online: 2019-04-21 Publish Date:2019-04-20
Abstract
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.Keywords: HDAC6,
Lipid droplets,
Metabolic adaption,
p62/SQSTM1,
Selective autophagy
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