Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 33, Issue 16, Pages 3180-3190Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00193-13
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Funding
- National Key Basic Research Project [2011CB910201, 2013CB530601]
- State Key Program of National Natural Science Foundation [31030048C120114]
- Shanghai Key Science and Technology Research Project [10JC1401000]
- National Natural Science Foundation [30870510, 31000603]
- Fudan University Ming-Dao Project for Graduate Students [EZF101336]
- Shanghai Leading Academic Discipline Project [B110]
- 985 Project [985 III-YFX0302]
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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 beta (C/EBP beta), an important adipogenic factor, is required for the activation of autophagy during 3T3-L1 adipocyte differentiation. An autophagy-related gene, Atg4b, is identified as a de novo target gene of C/EBP beta 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/EBP beta 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/EBP beta 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.
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