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RACK1 Promotes Autophagy by Enhancing the Atg14L-Beclin 1-Vps34-Vps15 Complex Formation upon Phosphorylation by AMPK

Yawei Zhao, Qingyang Wang, Guihua Qiu, Silei Zhou, Zhaofei Jing, Jingyang Wang, Wendie Wang, Junxia Cao, Kun Han, Qianqian Cheng, Beifen Shen, Yingyu Chen, Weiping J. Zhang, Yuanfang Ma, Jiyan Zhang

Research output: Contribution to journalArticlepeer-review

Abstract

Autophagy is essential for maintaining tissue homeostasis. Although adaptors have been demonstrated to facilitate the assembly of the Atg14L-Beclin 1-Vps34-Vps15 complex, which functions in autophagosome formation, it remains unknown whether the autophagy machinery actively recruits such adaptors. WD40-repeat proteins are a large, highly conserved family of adaptors implicated in various cellular activities. However, the role of WD40-repeat-only proteins, such as RACK1, in postnatal mammalian physiology remains unknown. Here, we report that hepatocyte-specific RACK1 deficiency leads to lipid accumulation in the liver, accompanied by impaired Atg14L-linked Vps34 activity and autophagy. Further exploration indicates that RACK1 participates in the formation of autophagosome biogenesis complex upon its phosphorylation by AMPK at Thr50. Thr50 phosphorylation of RACK1 enhances its direct binding to Vps15, Atg14L, and Beclin 1, thereby promoting the assembly of the autophagy-initiation complex. These observations provide insight into autophagy induction and establish a pivotal role for RACK1 in postnatal mammalian physiology.

Original languageEnglish (US)
Pages (from-to)1407-1417
Number of pages11
JournalCell Reports
Volume13
Issue number7
DOIs
StatePublished - Nov 17 2015

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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