Dysfunction of LSD-1 induces JNK signaling pathway-dependent abnormal development of thorax and apoptosis cell death in Drosophila melanogaster.

Perilipins are evolutionarily conserved from insects to mammals. Lipid storage droplet-1 (LSD-1) is a member of the lipid droplet's surface-binding protein family and counterpart to mammalian perilipin 1. The role of LSD-1 has already been reported in lipid metabolism of Drosophila. However, the function of this gene during specific tissue development is still under investigation. Here, we found that LSD-1 is expressed in the notum of the wing imaginal disc, and notum-specific knockdown of Lsd-1 by pannir-GAL4 driver leads to split thorax phenotype in adults, suggesting an essential role of LSD-1 in development of Drosophila thorax. As overexpression of JNK homolog, bsk (basket) suppresses Lsd-1 knockdown phenotype, the role of LSD-1 in thorax development was proved to be dependent on the activity of the Drosophila c-Jun N-terminal kinase (JNK). The puckered (puc) expression led to significant decrease in the JNK activity in wing discs of Lsd-1 knockdown flies. In addition, we also detected that depletion of Lsd-1 enhances apoptotic cell death in the wing notum area. Taken together, these data demonstrated that LSD-1 functions in Drosophila thorax development by regulating JNK pathway.