JAK/STAT signaling controls loss of polarity and apoptosis for elimination of supernumerary polar cells in the Drosophila ovary. Anne-Marie Pret^1,2, Antoine Borensztejn^1,3, Alba Torres^1,4, François Agnès^1,4. 1) Centre de Génétique Moléculaire, CNRS UPR3404, Gif-sur-Yvette, France; 2) Université de Versailles-St Quentin, Versailles, France; 3) Université Pierre et Marie Curie, Paris, France; 4) Université Paris-Sud, Orsay, France.

   Apoptosis is a widespread form of cell death, which allows precise destruction of cells preserving tissue architecture and integrity. Drosophila polar cells (PCs) are specialized pseudo-epithelial cells at ovarian follicle antero-posterior extremities, which are produced in excess (up to 6 cells) and restrict to exactly 2 cells by apoptosis. Reduction of PC number to 2 is necessary for subsequent recruitment of the correct number of border cells and their migration with PCs to the oocyte where they will form the micropyle, the sperm entry point into the oocyte. We have shown that supernumerary PC apoptosis is induced by cell autonomous and non-cell autonomous JAK/STAT-dependent activation of a canonical apoptosis cascade involving transcriptional activation of hid, leading to downregulation of Diap1 and consequent activation of executor caspases. Using cell polarity markers, we show that supernumerary PC elimination first involves full envelopment by neighboring PCs, accompanied by apical constriction with stereotyped anisotropy, concomitant with apical detachment followed by rounding up and shrinking. Our current work is aimed at establishing the molecular link(s) between JAK/STAT signaling, loss of PC polarity and PC apoptosis.