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A combinatorial code of identity transcription factors (iTFs) specifies the diversity of muscle types in  Drosophila . We previously showed that two iTFs, Lms and Ap, play critical role in the identity of a subset of larval body wall muscles, the lateral transverse (LT) muscles. Intriguingly, a small portion of  ap  and  lms  mutants displays an increased number of LT muscles, a phenotype that recalls pathological split muscle fibers in human. However, genes acting downstream of Ap and Lms to prevent these aberrant muscle feature are not known. Here, we applied a cell type specific translational profiling (TRAP) to identify gene expression signatures underlying identity of muscle subsets including the LT muscles. We found that  Gelsolin (Gel)  and  dCryAB , both encoding actin-interacting proteins, displayed LT muscle prevailing expression positively regulated by, the LT iTFs. Loss of  dCryAB  function resulted in LTs with irregular shape and occasional branched ends also observed in  ap  and  lms  mutant contexts. In contrast, enlarged and then split LTs with a greater number of myonuclei formed in  Gel  mutants while  Gel  gain of function resulted in unfused myoblasts, collectively indicating that  Gel  regulates LTs size and prevents splitting by limiting myoblast fusion. Thus,  dCryAB  and  Gel  act downstream of Lms and Ap and contribute to preventing LT muscle branching and splitting. Our findings offer first clues to still unknown mechanisms of pathological muscle splitting commonly detected in human dystrophic muscles and causing muscle weakness.

Gelsolin and dCryAB act downstream of muscle identity genes and contribute to preventing muscle splitting and branching in Drosophila