ATF3 induction prevents precocious activation of skeletal muscle stem cell by regulating H2B expression

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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Author(s)

  • Suyang Zhang
  • Feng Yang
  • Yile Huang
  • Liangqiang He
  • Yuying Li
  • Yingzhe Ding
  • Ting Xie
  • Hao Sun
  • Huating Wang

Detail(s)

Original languageEnglish
Article number4978
Journal / PublicationNature Communications
Volume14
Online published17 Aug 2023
Publication statusPublished - 2023

Link(s)

Abstract

Skeletal muscle stem cells (also called satellite cells, SCs) are important for maintaining muscle tissue homeostasis and damage-induced regeneration. However, it remains poorly understood how SCs enter cell cycle to become activated upon injury. Here we report that AP-1 family member ATF3 (Activating Transcription Factor 3) prevents SC premature activation. Atƒ3 is rapidly and transiently induced in SCs upon activation. Short-term deletion of Atƒ3 in SCs accelerates acute injury-induced regeneration, however, its long-term deletion exhausts the SC pool and thus impairs muscle regeneration. The Atf3 loss also provokes SC activation during voluntary exercise and enhances the activation during endurance exercise. Mechanistically, ATF3 directly activates the transcription of Histone 2B genes, whose reduction accelerates nucleosome displacement and gene transcription required for SC activation. Finally, the ATF3-dependent H2B expression also prevents genome instability and replicative senescence in SCs. Therefore, this study has revealed a previously unknown mechanism for preserving the SC population by actively suppressing precocious activation, in which ATF3 is a key regulator. © 2023, Springer Nature Limited.

Research Area(s)

Citation Format(s)

ATF3 induction prevents precocious activation of skeletal muscle stem cell by regulating H2B expression. / Zhang, Suyang; Yang, Feng; Huang, Yile et al.
In: Nature Communications, Vol. 14, 4978, 2023.

Research output: Journal Publications and Reviews (RGC: 21, 22, 62)21_Publication in refereed journalpeer-review

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