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Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms
Skeletal muscles play a central role in human movement through forces transmitted by contraction of the sarcomere. We recently showed that mammalian sarcomeres are connected through frequent branches forming a singular, mesh-like myofibrillar matrix. However, the extent to which myofibrillar connect...
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/PMC9106682/ https://www.ncbi.nlm.nih.gov/pubmed/35562354 http://dx.doi.org/10.1038/s41467-022-30401-9 |
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author | Ajayi, Peter T. Katti, Prasanna Zhang, Yingfan Willingham, T. Bradley Sun, Ye Bleck, Christopher K. E. Glancy, Brian |
author_facet | Ajayi, Peter T. Katti, Prasanna Zhang, Yingfan Willingham, T. Bradley Sun, Ye Bleck, Christopher K. E. Glancy, Brian |
author_sort | Ajayi, Peter T. |
collection | PubMed |
description | Skeletal muscles play a central role in human movement through forces transmitted by contraction of the sarcomere. We recently showed that mammalian sarcomeres are connected through frequent branches forming a singular, mesh-like myofibrillar matrix. However, the extent to which myofibrillar connectivity is evolutionarily conserved as well as mechanisms which regulate the specific architecture of sarcomere branching remain unclear. Here, we demonstrate the presence of a myofibrillar matrix in the tubular, but not indirect flight (IF) muscles within Drosophila melanogaster. Moreover, we find that loss of transcription factor H15 increases sarcomere branching frequency in the tubular jump muscles, and we show that sarcomere branching can be turned on in IF muscles by salm-mediated conversion to tubular muscles. Finally, we demonstrate that neurochondrin misexpression results in myofibrillar connectivity in IF muscles without conversion to tubular muscles. These data indicate an evolutionarily conserved myofibrillar matrix regulated by both cell-type dependent and independent mechanisms. |
format | Online Article Text |
id | pubmed-9106682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-91066822022-05-15 Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms Ajayi, Peter T. Katti, Prasanna Zhang, Yingfan Willingham, T. Bradley Sun, Ye Bleck, Christopher K. E. Glancy, Brian Nat Commun Article Skeletal muscles play a central role in human movement through forces transmitted by contraction of the sarcomere. We recently showed that mammalian sarcomeres are connected through frequent branches forming a singular, mesh-like myofibrillar matrix. However, the extent to which myofibrillar connectivity is evolutionarily conserved as well as mechanisms which regulate the specific architecture of sarcomere branching remain unclear. Here, we demonstrate the presence of a myofibrillar matrix in the tubular, but not indirect flight (IF) muscles within Drosophila melanogaster. Moreover, we find that loss of transcription factor H15 increases sarcomere branching frequency in the tubular jump muscles, and we show that sarcomere branching can be turned on in IF muscles by salm-mediated conversion to tubular muscles. Finally, we demonstrate that neurochondrin misexpression results in myofibrillar connectivity in IF muscles without conversion to tubular muscles. These data indicate an evolutionarily conserved myofibrillar matrix regulated by both cell-type dependent and independent mechanisms. Nature Publishing Group UK 2022-05-13 /pmc/articles/PMC9106682/ /pubmed/35562354 http://dx.doi.org/10.1038/s41467-022-30401-9 Text en © This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 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 Ajayi, Peter T. Katti, Prasanna Zhang, Yingfan Willingham, T. Bradley Sun, Ye Bleck, Christopher K. E. Glancy, Brian Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title | Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title_full | Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title_fullStr | Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title_full_unstemmed | Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title_short | Regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
title_sort | regulation of the evolutionarily conserved muscle myofibrillar matrix by cell type dependent and independent mechanisms |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9106682/ https://www.ncbi.nlm.nih.gov/pubmed/35562354 http://dx.doi.org/10.1038/s41467-022-30401-9 |
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