Muscle development and growth require myoblast fusion to form multinucleated muscle fibers. Several fusiogenic regulators have been identified that play vital roles in myoblast fusion in fish embryos. Loss-of- function (LOF) mutations in Jamb , JamC , Myomaker (Mymk ), and Myomixer (Mymx ) resulted in similar defective myoblast fusion and formation of mononucleated fibers in fish embryos. To investigate their LOF effects on fish muscle growth , we characterized the muscle phenotypes in adult zebrafish carrying single and double genetic mutations in jamb, jamc , mymk and mymx genes . We found that although myoblast fusion was compromised in zebrafish embryos of jamb and jamc single or jamb;jamc double mutants, these mutant fish showed no defect in muscle growth. The mutant fish were able to grow into adults that were indistinguishable from the wild-type sibling. In contrast, the adult mymk , mymx single, and jamb;mymk double mutants exhibited a stronger muscle phenotype compared to the jamb and jamc single and double mutants. The mymk and mymx single and jamb;mymk double mutants were smaller in size and weighed approximately one-third the weight of the wild type (WT) sibling. Single fiber analysis of adult skeletal myofibers revealed that jamb, jamc , or jamb;jamc mutants contained multinucleated myofibers with tens to hundreds of myonuclei per fiber , whereas mymk , mymx single and jamb;mymk double mutants contained mostly fibers with less than 10 nuclei per fiber . Significant intramuscular adipocyte infiltration was found in skeletal muscles of the mymk , mymx and jamb;mymk mutants . Collectively, these studies demonstrate that although Jamb, Jamc , Mymk and Mymx are all involved in myoblast fusion during early myogenesis, they have distinct roles in myoblast fusion during muscle growth. While Jamb and Jamc are dispensable for muscle growth , Mymk and Mymx are essential for myoblast fusion and muscle growth,