Actins are critical components of sarcomere structure and muscle function. Mammals and Drosophila each have six actin genes that exhibit distinct expression patterns spatially and temporally. Although the actins are highly conserved sequences they maintain distinct biochemical properties and affinities within the cell. Regardless, some of the actin isoforms can partially compensate for each other, making it unclear what the role of specific actin isoforms are during muscle formation and development. Therefore, using CRISPR technology we created two Drosophila actin mutants to determine the role of each actin in muscle development and function. Actin57B is a predominantly embryonic muscle actin isoform and Actin79B is the predominant actin isoform expressed in the Drosophila tergal depressor of the trochanter (TDT or jump) muscle. Mutations of each gene were created leading to null mutants. Through viability assays and structural analysis of embryonic muscles we determined that depletion of Actin57B results in an embryonic lethal phenotype with disrupted sarcomere structure. Although there is an increase in Actin87E mRNA by in situ hybridization, this increase is insufficient to rescue the sarcomere structural defects in Actin57B embryos. Actin79B deficient flies were structurally and functionally normal, showing a normal jumping ability despite the loss of the predominant jump muscle actin. This rescue of jump muscle function is due to compensation by low levels of Actin88F expression in the jump muscles. Double mutants deficient in both Actin79B and Actin88F show deficiencies in TDT muscle function. Therefore, Actin57B and Actin79B have distinct roles in muscle structure organization, however, Actin57B deficiency cannot be compensated for by increased levels of embryonic Actin87E while Actin79B deficiency is completely rescued by low levels of Actin88F. This demonstrates that secondary actin genes will expand their expression domain to compensate for deficiencies in other actin isoform, however, this genetic expansion does not necessarily translate to functional compensation.