Role of Zebrafish fhl1A in Satellite Cell and Skeletal Muscle Development

Title:Role of Zebrafish fhl1A in Satellite Cell and Skeletal Muscle Development

Volume: 17 Issue: 9

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

Affiliation:

• The Center for Heart Development, State Key Lab of Developmental Biology of Freshwater Fish, College of Life Sciences, Hunan Normal University, Changsha, Hunan 410081,China

• Guangdong Cardiovascular Institute, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou 510100,China

• The Center for Heart Development, State Key Lab of Developmental Biology of Freshwater Fish, College of Life Sciences, Hunan Normal University, Changsha, Hunan 410081,China

• The Center for Heart Development, State Key Lab of Developmental Biology of Freshwater Fish, College of Life Sciences, Hunan Normal University, Changsha, Hunan 410081,China

Keywords: fhl1A, satellite cells, skeletal muscle, development, zebrafish, myogenesis.

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.

Cite this article as:

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. *, Role of Zebrafish fhl1A in Satellite Cell and Skeletal Muscle Development, Current Molecular Medicine 2017; 17 (9) . https://dx.doi.org/10.2174/1566524018666180308113909