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The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism
Recent work has shown that Staufen1 plays key roles in skeletal muscle, yet little is known about its pattern of expression during embryonic and postnatal development. Here we first show that Staufen1 levels are abundant in mouse embryonic muscles and that its expression decreases thereafter, reachi...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230783/ https://www.ncbi.nlm.nih.gov/pubmed/25208565 http://dx.doi.org/10.1091/mbc.E14-04-0895 |
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author | Ravel-Chapuis, Aymeric Crawford, Tara E. Blais-Crépeau, Marie-Laure Bélanger, Guy Richer, Chase T. Jasmin, Bernard J. |
author_facet | Ravel-Chapuis, Aymeric Crawford, Tara E. Blais-Crépeau, Marie-Laure Bélanger, Guy Richer, Chase T. Jasmin, Bernard J. |
author_sort | Ravel-Chapuis, Aymeric |
collection | PubMed |
description | Recent work has shown that Staufen1 plays key roles in skeletal muscle, yet little is known about its pattern of expression during embryonic and postnatal development. Here we first show that Staufen1 levels are abundant in mouse embryonic muscles and that its expression decreases thereafter, reaching low levels in mature muscles. A similar pattern of expression is seen as cultured myoblasts differentiate into myotubes. Muscle degeneration/regeneration experiments revealed that Staufen1 increases after cardiotoxin injection before returning to the low levels seen in mature muscles. We next prevented the decrease in Staufen1 during differentiation by generating stable C2C12 muscle cell lines overexpressing Staufen1. Cells overexpressing Staufen1 differentiated poorly, as evidenced by reductions in the differentiation and fusion indices and decreases in MyoD, myogenin, MEF2A, and MEF2C, independently of Staufen-mediated mRNA decay. However, levels of c-myc, a factor known to inhibit differentiation, were increased in C2C12 cells overexpressing Staufen1 through enhanced translation. By contrast, the knockdown of Staufen1 decreased c-myc levels in myoblasts. Collectively our results show that Staufen1 is highly expressed during early stages of differentiation/development and that it can impair differentiation by regulating c-myc, thereby highlighting the multifunctional role of Staufen1 in skeletal muscle cells. |
format | Online Article Text |
id | pubmed-4230783 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-42307832015-01-30 The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism Ravel-Chapuis, Aymeric Crawford, Tara E. Blais-Crépeau, Marie-Laure Bélanger, Guy Richer, Chase T. Jasmin, Bernard J. Mol Biol Cell Articles Recent work has shown that Staufen1 plays key roles in skeletal muscle, yet little is known about its pattern of expression during embryonic and postnatal development. Here we first show that Staufen1 levels are abundant in mouse embryonic muscles and that its expression decreases thereafter, reaching low levels in mature muscles. A similar pattern of expression is seen as cultured myoblasts differentiate into myotubes. Muscle degeneration/regeneration experiments revealed that Staufen1 increases after cardiotoxin injection before returning to the low levels seen in mature muscles. We next prevented the decrease in Staufen1 during differentiation by generating stable C2C12 muscle cell lines overexpressing Staufen1. Cells overexpressing Staufen1 differentiated poorly, as evidenced by reductions in the differentiation and fusion indices and decreases in MyoD, myogenin, MEF2A, and MEF2C, independently of Staufen-mediated mRNA decay. However, levels of c-myc, a factor known to inhibit differentiation, were increased in C2C12 cells overexpressing Staufen1 through enhanced translation. By contrast, the knockdown of Staufen1 decreased c-myc levels in myoblasts. Collectively our results show that Staufen1 is highly expressed during early stages of differentiation/development and that it can impair differentiation by regulating c-myc, thereby highlighting the multifunctional role of Staufen1 in skeletal muscle cells. The American Society for Cell Biology 2014-11-15 /pmc/articles/PMC4230783/ /pubmed/25208565 http://dx.doi.org/10.1091/mbc.E14-04-0895 Text en © 2014 Ravel-Chapuis et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology. |
spellingShingle | Articles Ravel-Chapuis, Aymeric Crawford, Tara E. Blais-Crépeau, Marie-Laure Bélanger, Guy Richer, Chase T. Jasmin, Bernard J. The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title | The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title_full | The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title_fullStr | The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title_full_unstemmed | The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title_short | The RNA-binding protein Staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
title_sort | rna-binding protein staufen1 impairs myogenic differentiation via a c-myc–dependent mechanism |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4230783/ https://www.ncbi.nlm.nih.gov/pubmed/25208565 http://dx.doi.org/10.1091/mbc.E14-04-0895 |
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