Insulin signaling controls mitose/ endocycle switch through Notch signaling during drosophila oogenesis. Patrick Jouandin, Stéphane Noselli. Insitut Biologie Valrose (iBV), Nice, Alpes Maritimes (06), France.

   The insulin/ insulin-like growth factor signaling (IIS) pathway is evolutionary conserved among metazoans and couples growth, metabolism, stress response, lifespan and reproduction with nutrient availability. During drosophila oogenesis, IIS is important for germline and somatic follicular cells (FCs) growth and development, controlling germline cyst development, vitellogenesis, GSC division rates in response to neural insulin. In addition, IIS is responsible for the coupling of germline growth with FCs proliferation. However, the IIS effect on FCs proliferation seems indirect and mediated by the germline. Hence, the cell autonomous role of IIS within the follicular epithelium remains unclear. Following a proliferation phase, FCs undergo a stereotyped mitotic cell cycle/ endocycle (M/ E) switch that is critical for oogenesis. This process is achieved by a transient activation burst of the Notch (N) pathway activating Hindsigth (Hnt) which in turn inhibits Cut expression. This Cut down regulation is necessary and sufficient to promote the entry into endocycle. We investigated the cell autonomous role of IIS during this process. Interestingly, Drosophila Insulin Receptor (dinr) mutant clones entered the M/ E switch, but were unable to achieve it properly. Instead, dinr mutant clones were characterized by a lasting N activation concomitant with Cut misexpression. The results suggest that following poor diet conditions, IIS is required to maintain FC competence for further normal development, through an intermediate, switch-like state.