Abstract
Spermatogenesis is a conserved process across animals, involving the maintenance and differentiation of germ stem cells, haploid spermatid production via meiosis, and morphologically distinct sperm formation during spermiogenesis. We previously demonstrated that Slmap (Sarcolemma-associated protein) knockdown causes male sterility with no sperm in the seminal vesicle. Here, we show that Slmap knockdown in the early Drosophila melanogaster germline led to severe spermiogenesis defects, including aberrant paracrystalline material deposition in both mitochondrial derivatives, fusion of the two derivatives and of spermatids, loss of the central pair of axonemal microtubules, and axoneme clustering. These phenotypes were supported by transcriptomic data showing that the most prominently affected genes were those involved in cuticle development and plasma-membrane adhesion, including 20 cuticular protein genes. In parallel, we detected upregulation of individualization complex genes (chic, ctp, WASp, Lasp) and significant association with the oxidative phosphorylation pathway. Consistently, KEGG analysis and functional assays showed that the sustained damage activated germ cell apoptosis, as indicated by increased TUNEL signals, elevated Hid levels, and reduced Diap1 expression. Together, these findings place Slmap at the intersection of structural integrity and cell survival, linking its loss to both morphogenetic failure and activation of the Hid-Diap1 apoptotic pathway.
