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Smyd1b is required for skeletal and cardiac muscle function in zebrafish

Smyd1b is a member of the Smyd family that is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize Smyd1b function and its mechanism of action in myofibril...

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Detalles Bibliográficos
Autores principales: Li, Huiqing, Zhong, Yongwang, Wang, Zengfeng, Gao, Jie, Xu, Jin, Chu, Wuying, Zhang, Jianshe, Fang, Shenyun, Du, Shao Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The American Society for Cell Biology 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826989/
https://www.ncbi.nlm.nih.gov/pubmed/24068325
http://dx.doi.org/10.1091/mbc.E13-06-0352
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author Li, Huiqing
Zhong, Yongwang
Wang, Zengfeng
Gao, Jie
Xu, Jin
Chu, Wuying
Zhang, Jianshe
Fang, Shenyun
Du, Shao Jun
author_facet Li, Huiqing
Zhong, Yongwang
Wang, Zengfeng
Gao, Jie
Xu, Jin
Chu, Wuying
Zhang, Jianshe
Fang, Shenyun
Du, Shao Jun
author_sort Li, Huiqing
collection PubMed
description Smyd1b is a member of the Smyd family that is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize Smyd1b function and its mechanism of action in myofibrillogenesis, we analyzed the effects of smyd1b knockdown on myofibrillogenesis in skeletal and cardiac muscles of zebrafish embryos. The results show that knockdown of smyd1b causes significant disruption of myofibril organization in both skeletal and cardiac muscles of zebrafish embryos. Microarray and quantitative reverse transcription-PCR analyses show that knockdown of smyd1b up-regulates heat shock protein 90 (hsp90) and unc45b gene expression. Biochemical analysis reveals that Smyd1b can be coimmunoprecipitated with heat shock protein 90 α-1 and Unc45b, two myosin chaperones expressed in muscle cells. Consistent with its potential function in myosin folding and assembly, knockdown of smyd1b significantly reduces myosin protein accumulation without affecting mRNA expression. This likely results from increased myosin degradation involving unc45b overexpression. Together these data support the idea that Smyd1b may work together with myosin chaperones to control myosin folding, degradation, and assembly into sarcomeres during myofibrillogenesis.
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spelling pubmed-38269892014-01-30 Smyd1b is required for skeletal and cardiac muscle function in zebrafish Li, Huiqing Zhong, Yongwang Wang, Zengfeng Gao, Jie Xu, Jin Chu, Wuying Zhang, Jianshe Fang, Shenyun Du, Shao Jun Mol Biol Cell Articles Smyd1b is a member of the Smyd family that is specifically expressed in skeletal and cardiac muscles. Smyd1b plays a key role in thick filament assembly during myofibrillogenesis in skeletal muscles of zebrafish embryos. To better characterize Smyd1b function and its mechanism of action in myofibrillogenesis, we analyzed the effects of smyd1b knockdown on myofibrillogenesis in skeletal and cardiac muscles of zebrafish embryos. The results show that knockdown of smyd1b causes significant disruption of myofibril organization in both skeletal and cardiac muscles of zebrafish embryos. Microarray and quantitative reverse transcription-PCR analyses show that knockdown of smyd1b up-regulates heat shock protein 90 (hsp90) and unc45b gene expression. Biochemical analysis reveals that Smyd1b can be coimmunoprecipitated with heat shock protein 90 α-1 and Unc45b, two myosin chaperones expressed in muscle cells. Consistent with its potential function in myosin folding and assembly, knockdown of smyd1b significantly reduces myosin protein accumulation without affecting mRNA expression. This likely results from increased myosin degradation involving unc45b overexpression. Together these data support the idea that Smyd1b may work together with myosin chaperones to control myosin folding, degradation, and assembly into sarcomeres during myofibrillogenesis. The American Society for Cell Biology 2013-11-15 /pmc/articles/PMC3826989/ /pubmed/24068325 http://dx.doi.org/10.1091/mbc.E13-06-0352 Text en © 2013 Li 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 of Cell Biology.
spellingShingle Articles
Li, Huiqing
Zhong, Yongwang
Wang, Zengfeng
Gao, Jie
Xu, Jin
Chu, Wuying
Zhang, Jianshe
Fang, Shenyun
Du, Shao Jun
Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title_full Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title_fullStr Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title_full_unstemmed Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title_short Smyd1b is required for skeletal and cardiac muscle function in zebrafish
title_sort smyd1b is required for skeletal and cardiac muscle function in zebrafish
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826989/
https://www.ncbi.nlm.nih.gov/pubmed/24068325
http://dx.doi.org/10.1091/mbc.E13-06-0352
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