Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila
Abstract A combinatorial code of identity transcription factors (iTFs) specifies the diversity of muscle types in Drosophila. We previously showed that two iTFs, Lms and Ap, play critical role in the identity of a subset of larval body wall muscles, the lateral transverse (LT) muscles. Intriguingly,...
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doaj-815fbc9e76604d64817d6a652c3683ac2021-06-27T11:30:12ZengNature Publishing GroupScientific Reports2045-23222021-06-0111111310.1038/s41598-021-92506-3Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in DrosophilaBenjamin Bertin0Yoan Renaud1Teresa Jagla2Guillaume Lavergne3Cristiana Dondi4Jean-Philippe Da Ponte5Guillaume Junion6Krzysztof Jagla7GReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneGReD Institute - INSERM U1103, CNRS UMR6293, Université Clermont AuvergneAbstract A combinatorial code of identity transcription factors (iTFs) specifies the diversity of muscle types in Drosophila. We previously showed that two iTFs, Lms and Ap, play critical role in the identity of a subset of larval body wall muscles, the lateral transverse (LT) muscles. Intriguingly, a small portion of ap and lms mutants displays an increased number of LT muscles, a phenotype that recalls pathological split muscle fibers in human. However, genes acting downstream of Ap and Lms to prevent these aberrant muscle feature are not known. Here, we applied a cell type specific translational profiling (TRAP) to identify gene expression signatures underlying identity of muscle subsets including the LT muscles. We found that Gelsolin (Gel) and dCryAB, both encoding actin-interacting proteins, displayed LT muscle prevailing expression positively regulated by, the LT iTFs. Loss of dCryAB function resulted in LTs with irregular shape and occasional branched ends also observed in ap and lms mutant contexts. In contrast, enlarged and then split LTs with a greater number of myonuclei formed in Gel mutants while Gel gain of function resulted in unfused myoblasts, collectively indicating that Gel regulates LTs size and prevents splitting by limiting myoblast fusion. Thus, dCryAB and Gel act downstream of Lms and Ap and contribute to preventing LT muscle branching and splitting. Our findings offer first clues to still unknown mechanisms of pathological muscle splitting commonly detected in human dystrophic muscles and causing muscle weakness.https://doi.org/10.1038/s41598-021-92506-3 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Benjamin Bertin Yoan Renaud Teresa Jagla Guillaume Lavergne Cristiana Dondi Jean-Philippe Da Ponte Guillaume Junion Krzysztof Jagla |
spellingShingle |
Benjamin Bertin Yoan Renaud Teresa Jagla Guillaume Lavergne Cristiana Dondi Jean-Philippe Da Ponte Guillaume Junion Krzysztof Jagla Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila Scientific Reports |
author_facet |
Benjamin Bertin Yoan Renaud Teresa Jagla Guillaume Lavergne Cristiana Dondi Jean-Philippe Da Ponte Guillaume Junion Krzysztof Jagla |
author_sort |
Benjamin Bertin |
title |
Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila |
title_short |
Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila |
title_full |
Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila |
title_fullStr |
Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila |
title_full_unstemmed |
Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila |
title_sort |
gelsolin and dcryab act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in drosophila |
publisher |
Nature Publishing Group |
series |
Scientific Reports |
issn |
2045-2322 |
publishDate |
2021-06-01 |
description |
Abstract A combinatorial code of identity transcription factors (iTFs) specifies the diversity of muscle types in Drosophila. We previously showed that two iTFs, Lms and Ap, play critical role in the identity of a subset of larval body wall muscles, the lateral transverse (LT) muscles. Intriguingly, a small portion of ap and lms mutants displays an increased number of LT muscles, a phenotype that recalls pathological split muscle fibers in human. However, genes acting downstream of Ap and Lms to prevent these aberrant muscle feature are not known. Here, we applied a cell type specific translational profiling (TRAP) to identify gene expression signatures underlying identity of muscle subsets including the LT muscles. We found that Gelsolin (Gel) and dCryAB, both encoding actin-interacting proteins, displayed LT muscle prevailing expression positively regulated by, the LT iTFs. Loss of dCryAB function resulted in LTs with irregular shape and occasional branched ends also observed in ap and lms mutant contexts. In contrast, enlarged and then split LTs with a greater number of myonuclei formed in Gel mutants while Gel gain of function resulted in unfused myoblasts, collectively indicating that Gel regulates LTs size and prevents splitting by limiting myoblast fusion. Thus, dCryAB and Gel act downstream of Lms and Ap and contribute to preventing LT muscle branching and splitting. Our findings offer first clues to still unknown mechanisms of pathological muscle splitting commonly detected in human dystrophic muscles and causing muscle weakness. |
url |
https://doi.org/10.1038/s41598-021-92506-3 |
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