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Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape
Muscle stem cells (MuSCs) are essential for skeletal muscle development and regeneration, ensuring muscle integrity and normal function. The myogenic proliferation and differentiation of MuSCs are orchestrated by a cascade of transcription factors. In this study, we elucidate the specific role of tr...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9646716/ https://www.ncbi.nlm.nih.gov/pubmed/36352000 http://dx.doi.org/10.1038/s42003-022-04176-0 |
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author | Wang, Sheng Liao, Yinlong Zhang, Haoyuan Jiang, Yunqi Peng, Zhelun Ren, Ruimin Li, Xinyun Wang, Heng |
author_facet | Wang, Sheng Liao, Yinlong Zhang, Haoyuan Jiang, Yunqi Peng, Zhelun Ren, Ruimin Li, Xinyun Wang, Heng |
author_sort | Wang, Sheng |
collection | PubMed |
description | Muscle stem cells (MuSCs) are essential for skeletal muscle development and regeneration, ensuring muscle integrity and normal function. The myogenic proliferation and differentiation of MuSCs are orchestrated by a cascade of transcription factors. In this study, we elucidate the specific role of transcription factor 12 (Tcf12) in muscle development and regeneration based on loss-of-function studies. Muscle-specific deletion of Tcf12 cause muscle weight loss owing to the reduction of myofiber size during development. Inducible deletion of Tcf12 specifically in adult MuSCs delayed muscle regeneration. The examination of MuSCs reveal that Tcf12 deletion resulted in cell-autonomous defects during myogenesis and Tcf12 is necessary for proper myogenic gene expression. Mechanistically, TCF12 and MYOD work together to stabilise chromatin conformation and sustain muscle cell fate commitment-related gene and chromatin architectural factor expressions. Altogether, our findings identify Tcf12 as a crucial regulator of MuSCs chromatin remodelling that regulates muscle cell determination and participates in skeletal muscle development and regeneration. |
format | Online Article Text |
id | pubmed-9646716 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-96467162022-11-15 Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape Wang, Sheng Liao, Yinlong Zhang, Haoyuan Jiang, Yunqi Peng, Zhelun Ren, Ruimin Li, Xinyun Wang, Heng Commun Biol Article Muscle stem cells (MuSCs) are essential for skeletal muscle development and regeneration, ensuring muscle integrity and normal function. The myogenic proliferation and differentiation of MuSCs are orchestrated by a cascade of transcription factors. In this study, we elucidate the specific role of transcription factor 12 (Tcf12) in muscle development and regeneration based on loss-of-function studies. Muscle-specific deletion of Tcf12 cause muscle weight loss owing to the reduction of myofiber size during development. Inducible deletion of Tcf12 specifically in adult MuSCs delayed muscle regeneration. The examination of MuSCs reveal that Tcf12 deletion resulted in cell-autonomous defects during myogenesis and Tcf12 is necessary for proper myogenic gene expression. Mechanistically, TCF12 and MYOD work together to stabilise chromatin conformation and sustain muscle cell fate commitment-related gene and chromatin architectural factor expressions. Altogether, our findings identify Tcf12 as a crucial regulator of MuSCs chromatin remodelling that regulates muscle cell determination and participates in skeletal muscle development and regeneration. Nature Publishing Group UK 2022-11-09 /pmc/articles/PMC9646716/ /pubmed/36352000 http://dx.doi.org/10.1038/s42003-022-04176-0 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Wang, Sheng Liao, Yinlong Zhang, Haoyuan Jiang, Yunqi Peng, Zhelun Ren, Ruimin Li, Xinyun Wang, Heng Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title | Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title_full | Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title_fullStr | Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title_full_unstemmed | Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title_short | Tcf12 is required to sustain myogenic genes synergism with MyoD by remodelling the chromatin landscape |
title_sort | tcf12 is required to sustain myogenic genes synergism with myod by remodelling the chromatin landscape |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9646716/ https://www.ncbi.nlm.nih.gov/pubmed/36352000 http://dx.doi.org/10.1038/s42003-022-04176-0 |
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