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Histone demethylase JMJD1A coordinates acute and chronic adaptation to cold stress via thermogenic phospho-switch

Author

Listed:
  • Yohei Abe

    (The University of Tokyo)

  • Yosuke Fujiwara

    (The University of Tokyo)

  • Hiroki Takahashi

    (The University of Tokyo)

  • Yoshihiro Matsumura

    (The University of Tokyo)

  • Tomonobu Sawada

    (The University of Tokyo)

  • Shuying Jiang

    (Niigata College of Medical Technology)

  • Ryo Nakaki

    (Rhelixa Inc.
    The University of Tokyo)

  • Aoi Uchida

    (The University of Tokyo)

  • Noriko Nagao

    (The University of Tokyo)

  • Makoto Naito

    (Niigata Medical Center)

  • Shingo Kajimura

    (University of California, San Francisco)

  • Hiroshi Kimura

    (Tokyo Institute of Technology)

  • Timothy F. Osborne

    (Sanford-Burnham Medical Research Institute)

  • Hiroyuki Aburatani

    (The University of Tokyo)

  • Tatsuhiko Kodama

    (The University of Tokyo)

  • Takeshi Inagaki

    (The University of Tokyo
    Gunma University)

  • Juro Sakai

    (The University of Tokyo
    Tohoku University Graduate School of Medicine)

Abstract

In acute cold stress in mammals, JMJD1A, a histone H3 lysine 9 (H3K9) demethylase, upregulates thermogenic gene expressions through β-adrenergic signaling in brown adipose tissue (BAT). Aside BAT-driven thermogenesis, mammals have another mechanism to cope with long-term cold stress by inducing the browning of the subcutaneous white adipose tissue (scWAT). Here, we show that this occurs through a two-step process that requires both β-adrenergic-dependent phosphorylation of S265 and demethylation of H3K9me2 by JMJD1A. The histone demethylation-independent acute Ucp1 induction in BAT and demethylation-dependent chronic Ucp1 expression in beige scWAT provides complementary molecular mechanisms to ensure an ordered transition between acute and chronic adaptation to cold stress. JMJD1A mediates two major signaling pathways, namely, β-adrenergic receptor and peroxisome proliferator-activated receptor-γ (PPARγ) activation, via PRDM16-PPARγ-P-JMJD1A complex for beige adipogenesis. S265 phosphorylation of JMJD1A, and the following demethylation of H3K9me2 might prove to be a novel molecular target for the treatment of metabolic disorders, via promoting beige adipogenesis.

Suggested Citation

  • Yohei Abe & Yosuke Fujiwara & Hiroki Takahashi & Yoshihiro Matsumura & Tomonobu Sawada & Shuying Jiang & Ryo Nakaki & Aoi Uchida & Noriko Nagao & Makoto Naito & Shingo Kajimura & Hiroshi Kimura & Timo, 2018. "Histone demethylase JMJD1A coordinates acute and chronic adaptation to cold stress via thermogenic phospho-switch," Nature Communications, Nature, vol. 9(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-03868-8
    DOI: 10.1038/s41467-018-03868-8
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    Cited by:

    1. Hiroki Takahashi & Ge Yang & Takeshi Yoneshiro & Yohei Abe & Ryo Ito & Chaoran Yang & Junna Nakazono & Mayumi Okamoto-Katsuyama & Aoi Uchida & Makoto Arai & Hitomi Jin & Hyunmi Choi & Myagmar Tumenjar, 2022. "MYPT1-PP1β phosphatase negatively regulates both chromatin landscape and co-activator recruitment for beige adipogenesis," Nature Communications, Nature, vol. 13(1), pages 1-19, December.

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