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

Yuqin Wang, Ming Gao, Fuxing Zhu, Xinzhi Li, Ying Yang, Qiuxin Yan, Linna Jia, Liwei Xie and Zheng Chen ()
Additional contact information
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

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: 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.

Date: 2020
References: Add references at CitEc
Citations: View citations in EconPapers (4)

Downloads: (external link)
https://www.nature.com/articles/s41467-020-15488-2 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-15488-2

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-020-15488-2

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().