Transactivation of atg4b by c/ebp promotes autophagy to facilitate adipogenesis

Liang Guo, Jia Xin Huang, Yuan Liu, Xi Li, Shui Rong Zhou, Shu Wen Qian, Yang Liu, Hao Zhu, Hai Yan Huang, Y. J. Dang, Qi Qun Tang

Research output: Contribution to journalArticlepeer-review

Abstract

Autophagy is a highly conserved self-digestion pathway involved in various physiological and pathophysiological processes. Recent studies have implicated a pivotal role of autophagy in adipocyte differentiation, but the molecular mechanism for its role and how it is regulated during this process are not clear. Here, we show that CCAAT/enhancer-binding protein β (C/EBPβ), an important adipogenic factor, is required for the activation of autophagy during 3T3-L1 adipocyte differentiation. An autophagyrelated gene, Atg4b, is identified as a de novo target gene of C/EBPβ and is shown to play an important role in 3T3-L1 adipocyte differentiation. Furthermore, autophagy is required for the degradation of Klf2 and Klf3, two negative regulators of adipocyte differentiation, which is mediated by the adaptor protein p62/SQSTM1. Importantly, the regulation of autophagy by C/EBPβ and the role of autophagy in Klf2/3 degradation and in adipogenesis are further confirmed in mouse models. Our data describe a novel function of C/EBPβ in regulating autophagy and reveal the mechanism of autophagy during adipocyte differentiation. These new insights into the molecular mechanism of adipose tissue development provide a functional pathway with therapeutic potential against obesity and its related metabolic disorders

Original languageEnglish (US)
Pages (from-to)3180-3190
Number of pages11
JournalMolecular and cellular biology
Volume33
Issue number16
DOIs
StatePublished - 2013

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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