HDAC6 regulates lipid droplet turnover in response to nutrient deprivation via p62-mediated selective autophagy
Autor: | Yuanhang Xiang, Chuanxian Wei, Renjie Jiao, Hao Wang, Xuehong Liang, Yan Yan, Chung-Weng Phang |
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Rok vydání: | 2019 |
Předmět: |
Regulator
Biology Diet High-Fat Histone Deacetylase 6 03 medical and health sciences 0302 clinical medicine Sequestosome 1 Lipid droplet Organelle Autophagy Genetics Animals Drosophila Proteins education Molecular Biology 030304 developmental biology TATA-Binding Protein Associated Factors 0303 health sciences education.field_of_study Lipid metabolism Lipid Droplets Nutrients HDAC6 Cell biology Protein Transport Drosophila melanogaster Aggresome Transcription Factor TFIID 030217 neurology & neurosurgery |
Zdroj: | Journal of Genetics and Genomics. 46:221-229 |
ISSN: | 1673-8527 |
Popis: | 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. |
Databáze: | OpenAIRE |
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