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Linc-MYH 通过调控 INO80 来调节肌肉干细胞数量和骨骼肌肥大。

Linc-MYH configures INO80 to regulate muscle stem cell numbers and skeletal muscle hypertrophy.

机构信息

Department of Cardiac Development and Remodelling, Max Planck Institute for Heart- and Lung Research, Bad Nauheim, Germany.

Max Planck Institute for Heart- and Lung Research, FACS Service Group, Bad Nauheim, Germany.

出版信息

EMBO J. 2020 Nov 16;39(22):e105098. doi: 10.15252/embj.2020105098. Epub 2020 Sep 22.

DOI:10.15252/embj.2020105098
PMID:32960481
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7667881/
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.

摘要

染色质重塑复合物在转录调控和染色体维持中具有功能，但这些通常普遍存在的复合物的功能如何在细胞环境中特异性指定，在很大程度上仍然未知。在这里，我们描述了进化上保守的长非编码 RNA linc-MYH 调节肌干细胞中 INO80 染色质重塑复合物的组成，并防止其与 WDR5 和转录因子 YY1 相互作用。linc-MYH 作为一种选择性的分子开关在转录中起作用，它控制着普遍存在的 INO80 复合物的促增殖功能，但不影响其在维持基因组稳定性方面的作用。该分子开关对于限制静止的 MuSCs 的产生和肌细胞在体内平衡和再生过程中的增殖是必不可少的。由于 linc-MYH 在增殖的肌细胞中表达，但不在静止的 MuSCs 中表达，因此我们认为肌细胞的增殖程度对静止的 MuSC 池的大小具有决定性的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/d423d5d40307/EMBJ-39-e105098-g011.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/a67525e84416/EMBJ-39-e105098-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/a473ac889a28/EMBJ-39-e105098-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/58e4f7eb5b7f/EMBJ-39-e105098-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/da4829701ed3/EMBJ-39-e105098-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/f4f8a4b745b9/EMBJ-39-e105098-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/6594f6a6d505/EMBJ-39-e105098-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/1d1a6b01aa72/EMBJ-39-e105098-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/d423d5d40307/EMBJ-39-e105098-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/cde91e274ad4/EMBJ-39-e105098-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/af8e24763659/EMBJ-39-e105098-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/f93dc756ada3/EMBJ-39-e105098-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/a67525e84416/EMBJ-39-e105098-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/a473ac889a28/EMBJ-39-e105098-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/58e4f7eb5b7f/EMBJ-39-e105098-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/da4829701ed3/EMBJ-39-e105098-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/f4f8a4b745b9/EMBJ-39-e105098-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/6594f6a6d505/EMBJ-39-e105098-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/1d1a6b01aa72/EMBJ-39-e105098-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc60/7667881/d423d5d40307/EMBJ-39-e105098-g011.jpg

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