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MED20 is a non-essential subunit of the transcriptional coactivator Mediator complex, but its physiological function remains largely unknown. Here, we identify MED20 as a substrate of the anti-obesity CRL4-WDTC1 E3 ubiquitin ligase complex through affinity purification and candidate screening. Overexpression of WDTC1 leads to degradation of MED20, whereas depletion of WDTC1 or CUL4A/B causes accumulation of MED20. Depleting MED20 inhibits adipogenesis, and a non-degradable MED20 mutant restores adipogenesis in WDTC1-overexpressing cells. Furthermore, knockout of Med20 in preadipocytes abolishes development of brown adipose tissues. Removing one allele of Med20 in preadipocytes protects mice from diet-induced obesity and reverses weight gain in Cul4a- or Cul4b-depleted mice. Chromatin immunoprecipitation sequencing (ChIP-seq) analysis reveals that MED20 organizes the early adipogenic complex by bridging C/EBPβ and RNA polymerase II to promote transcription of the central adipogenic factor, PPARγ. Our findings have thus uncovered a critical role of MED20 in promoting adipogenesis, development of adipose tissue and diet-induced obesity. Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.


Wen-Shuai Tang, Li Weng, Xu Wang, Chang-Qin Liu, Guo-Sheng Hu, Shu-Ting Yin, Ying Tao, Ni-Na Hong, Huiling Guo, Wen Liu, Hong-Rui Wang, Tong-Jin Zhao. The Mediator subunit MED20 organizes the early adipogenic complex to promote development of adipose tissues and diet-induced obesity. Cell reports. 2021 Jul 06;36(1):109314

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PMID: 34233190

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