Nucleoporin107 is a major contributor to soma-germline communication, essential for ovarian development and function

We recently identified a missense mutation in Nucleoporin107 (Nup107; D447N) underlying XX-ovarian-dysgenesis, a rare disorder characterized by underdeveloped and dysfunctional ovaries. Modeling of the human mutation in Drosophila or specific knockdown of Nup107 in the gonadal soma resulted in ovarian-dysgenesis-like phenotypes. In the adult ovaries the secreted BMP ligand emanating from the terminal filament and cap cells niche maintains the stemness of the adjacent germline stem cells (GSCs). Escort cells (ECs) and their cellular processes encapsulate the GSC daughter cells and restrict the BMP signal, thus allowing for further differentiation and production of fertile oocytes. Interestingly, EGF signal secreted by the germ cells induce in the responsive ECs the formation of their extensions and repression of Dally, a presenter of the BMP signal. Both actions are required for restricting the BMP signal. We have found that flies harboring the corresponding human mutation or gonadal somatic knockdown of Nup107 leads to loss of EGFR signaling in ECs. Consequently, the affected ECs lose their extensions and ectopically express Dally. This data reveals the function of Nup107 as a key contributor to soma-germline communication where it regulates EGFR signaling in ECs. In turn, EGFR signaling regulates BMP through two independent methods: by repressing Dally and ending BMP presentation to differentiating germ cells, as well as blocking the formation of the cellular extensions.