학술논문
Linc-MYH configures INO80 to regulate muscle stem cell numbers and skeletal muscle hypertrophy.
Document Type
Academic Journal
Author
Schutt C; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Hallmann A; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Hachim S; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Klockner I; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Valussi M; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Atzberger A; Max Planck Institute for Heart- and Lung Research, FACS Service Group, Bad Nauheim, Germany.; Graumann J; Max Planck Institute for Heart- and Lung Research, Mass Spectrometry Service Group, Bad Nauheim, Germany.; Braun T; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.; Boettger T; Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.
Source
Publisher: Wiley Blackwell Country of Publication: England NLM ID: 8208664 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2075 (Electronic) Linking ISSN: 02614189 NLM ISO Abbreviation: EMBO J Subsets: MEDLINE
Subject
Language
English
Abstract
Chromatin remodeling complexes have functions in transcriptional regulation and chromosome maintenance, but it is mostly unknown how the function of these normally ubiquitous complexes is specified in the cellular context. Here, we describe that the evolutionary conserved long non-coding RNA linc-MYH regulates the composition of the INO80 chromatin remodeler complex in muscle stem cells and prevents interaction with WDR5 and the transcription factor YY1. Linc-MYH acts as a selective molecular switch in trans that governs the pro-proliferative function of the ubiquitous INO80 complex but does not affect its role in maintaining genomic stability. The molecular switch is essential for restricting generation of quiescent MuSCs and proliferation of myoblasts in homeostasis and regeneration. Since linc-MYH is expressed in proliferating myoblasts but not in quiescent MuSCs, we reason that the extent of myoblast proliferation has decisive effects on the size of the quiescent MuSC pool.
(© 2020 The Authors. Published under the terms of the CC BY NC ND 4.0 license.)
(© 2020 The Authors. Published under the terms of the CC BY NC ND 4.0 license.)