Synergistic actions of Nup43 and Myosin VI drive actin cone assembly during <i>Drosophila</i> spermiogenesis

Nuclear pore complexes, composed of nucleoporins (Nups), are critical for bidirectional nucleocytoplasmic transport and regulate various cellular processes, thus contributing significantly to organismal development. Intriguingly, the integral Nup107 complex member, Nup43, is linked with premature ovarian insufficiency. Here, we report that Nup43 plays essential roles in Drosophila fertility, and Nup43 null mutant females and males are sterile. In mutant females, after fertilization with wildtype, mitotic progression during embryonic development is severely disrupted at early divisions, leading to irregular mitotic divisions. However, male sterility results from sperm development arrest at the canoe stage. In Nup43 mutants, sperm maturation is suspended, and nuclear elongation, nuclear shaping, and actin cone assembly aspects of individualization complex formation are adversely affected. Further, the Nup43 transgene completely rescues spermiogenesis defects in mutants. Myosin VI (jar), an actin-based motor, interacts with Nup43 and rescues the actin cone assembly but not the sterility defects seen in Nup43 null mutants. In essence, we report a novel non-canonical function for Nup43 in Drosophila fertility and spermiogenesis and propose that Nup43 facilitates sperm individualization by promoting jar-dependent actin cone assembly.