Asymmetric cell division (ACD) is a conserved mechanism by which cell fate diversity is generated during development and throughout adult life. How a cell can produce two daughter cells with different identities and how defects in this asymmetry contribute to diseases are the fundamental questions we study using the Drosophila adult sensory organ (SO) lineage as a model system. SO Precursors (SOP) are epithelial cells present in a single layer neuroepithelium on the dorsal thorax of Drosophila. SOP undergoes a series of four ACD in which a mother cell gives rise to two daughter cells via uneven segregation of the Notch regulators Numb and Neuralized. Thus, at each division, the acquisition of cell identity is controlled by the differential activation of Notch. Notch is activated by Delta (Dl) present on the surface of adjacent cells. Our recent work contributed to show that sorting of N and Dl along the apico-basal axis at the exit of mitosis is important for proper N activation. We identified new regulators of N signaling following asymmetric cell division including membrane traffic regulators (AP-1) and regulators of epithelial cell cytokinesis (septins). We investigate the molecular mechanisms by which AP-1 and septins controls N signaling by studying: - novel AP-1 interacting factors and traffic regulators identified by genetic and biochemical means, - the role of AP- 1 on the transport of E-Cadherin (E-Cad), - the role of AP-1 and E-Cad in the organization of N signaling platform, - the remodeling of the junctions and the maintenance of epithelial cell polarity throughout ACD.
Our research is currently funded by the CNRS, ANR Programme Blanc ApiNotch 2012-2015, La ligue Nationale contre le Cancer-Equipe Labellisée