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METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice

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  • Yuqin Wang

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Ming Gao

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Fuxing Zhu

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Xinzhi Li

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Ying Yang

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Qiuxin Yan

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

  • Linna Jia

    (Northeast Normal University)

  • Liwei Xie

    (State Key Laboratory of Applied Microbiology Southern China, Guangdong Provincial Key Laboratory of Microbial Culture Collection and Application, Guangdong Open Laboratory of Applied Microbiology, Guangdong Institute of Microbiology, Guangdong Academy of Sciences)

  • Zheng Chen

    (HIT Center for Life Sciences, School of Life Science and Technology, Harbin Institute of Technology)

Abstract

Brown adipose tissue (BAT) undergoes rapid postnatal development and then protects against cold and obesity into adulthood. However, the molecular mechanism that determines postnatal development and maturation of BAT is largely unknown. Here we show that METTL3 (a key RNA methyltransferase) expression increases significantly in interscapular brown adipose tissue (iBAT) after birth and plays an essential role in the postnatal development and maturation of iBAT. BAT-specific deletion of Mettl3 severely impairs maturation of BAT in vivo by decreasing m6A modification and expression of Prdm16, Pparg, and Ucp1 transcripts, which leads to a marked reduction in BAT-mediated adaptive thermogenesis and promotes high-fat diet (HFD)-induced obesity and systemic insulin resistance. These data demonstrate that METTL3 is an essential regulator that controls iBAT postnatal development and energy homeostasis.

Suggested Citation

  • Yuqin Wang & Ming Gao & Fuxing Zhu & Xinzhi Li & Ying Yang & Qiuxin Yan & Linna Jia & Liwei Xie & Zheng Chen, 2020. "METTL3 is essential for postnatal development of brown adipose tissue and energy expenditure in mice," Nature Communications, Nature, vol. 11(1), pages 1-14, December.
  • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-15488-2
    DOI: 10.1038/s41467-020-15488-2
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    Cited by:

    1. Sujun Yan & Xiaoling Zhou & Canlan Wu & Yunyi Gao & Yu Qian & Jingyu Hou & Renxiang Xie & Bing Han & Zhanghui Chen & Saisai Wei & Xiangwei Gao, 2023. "Adipocyte YTH N(6)-methyladenosine RNA-binding protein 1 protects against obesity by promoting white adipose tissue beiging in male mice," Nature Communications, Nature, vol. 14(1), pages 1-13, December.
    2. Xinzhi Li & Kaixin Ding & Xueying Li & Bingchuan Yuan & Yuqin Wang & Zhicheng Yao & Shuaikang Wang & He Huang & Bolin Xu & Liwei Xie & Tuo Deng & Xiao-wei Chen & Zheng Chen, 2022. "Deficiency of WTAP in hepatocytes induces lipoatrophy and non-alcoholic steatohepatitis (NASH)," Nature Communications, Nature, vol. 13(1), pages 1-19, December.
    3. Xinzhi Li & Bingchuan Yuan & Min Lu & Yuqin Wang & Na Ding & Chunhong Liu & Ming Gao & Zhicheng Yao & Shiyan Zhang & Yujun Zhao & Liwei Xie & Zheng Chen, 2021. "The methyltransferase METTL3 negatively regulates nonalcoholic steatohepatitis (NASH) progression," Nature Communications, Nature, vol. 12(1), pages 1-17, December.

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