Four-and-a-half LIM protein FHL1 mutations are associated with human myopathies.However,the function of this protein in skeletal development remains unclear.Zebrafish fhlA is the only known homolog of human FHL1.Here,we showed that fhlA knockdown causes defective skeletal muscle development.The defects can be largely rescued in the fhlA mophants injected with the fhlA mRNA.We also showed that fhlA affected the number of satellite cells.The decrease in the number of satellite cells and the emergence of skeletal muscle abnormality were associated with alterations in the gene expression of myoD,pax7,mef2ca,and skMLCK.We also showed that endogenous fhlA expression in skeletal muscles could be modulated by RA signaling and both fhlA and RA signaling caused similar skeletal muscle development phenotypes,suggesting that the role of fhlA in skeletal myogenesis was probably regulated by RA signaling.Taken together,our data suggest that fhlA is required for regulation of the number of satellite cells and for skeletal myogenesis in vivo.