Role of Zebrafish fhl1A in Satellite Cell and Skeletal Muscle Development.

Abstract:

BACKGROUND:Four-and-a-half LIM domains protein 1 (FHL1) mutations are associated with human myopathies. However, the function of this protein in skeletal development remains unclear. METHODS:Whole-mount in situ hybridization and embryo immunostaining were performed. RESULTS:Zebrafish Fhl1A is the homologue of human FHL1. We showed that fhl1A knockdown causes defective skeletal muscle development, while injection with fhl1A mRNA largely recovered the muscle development in these fhl1A morphants. We also demonstrated that fhl1A knockdown decreases the number of satellite cells. This decrease in satellite cells and the emergence of skeletal muscle abnormalities were associated with alterations in the gene expression of myoD, pax7, mef2ca and skMLCK. We also demonstrated that fhl1A expression and retinoic acid (RA) signalling caused similar skeletal muscle development phenotypes. Moreover, when treated with exogenous RA, endogenous fhl1A expression in skeletal muscles was robust. When treated with DEAB, an RA signalling inhibitor which inhibits the activity of retinaldehyde dehydrogenase, fhl1A was downregulated. CONCLUSION:fhl1A functions as an activator in regulating the number of satellite cells and in skeletal muscle development. The role of fhl1A in skeletal myogenesis is regulated by RA signaling.

journal_name

Curr Mol Med

authors

Chen F,Yuan W,Mo X,Zhuang J,Wang Y,Chen J,Jiang Z,Zhu X,Zeng Q,Wan Y,Li F,Shi Y,Cao L,Fan X,Luo S,Ye X,Chen Y,Dai G,Gao J,Wang X,Xie H,Zhu P,Li Y,Wu X

doi

10.2174/1566524018666180308113909

subject

Has Abstract

pub_date

2017-01-01 00:00:00

pages

627-636

issue

9

eissn

1566-5240

issn

1875-5666

pii

CMM-EPUB-88986

journal_volume

17

pub_type

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