Clathrin adaptor AP-1 and Stratum act in parallel pathways to control Notch activation in Drosophila Sensory Organ Precursor Cells

Abstract

Drosophila sensory organ precursors divide asymmetrically to generate pIIa/pIIb cells whose identity relies on activation of Notch at cytokinesis. While Notch is present apically and basally relative to the midbody at the pIIa-pIIb interface, the basal pool of Notch is reported to be the main contributor for Notch activation in the pIIa cell. Intra-lineage signaling requires appropriate apico-basal targeting of Notch, its ligand Delta and its trafficking partner Sanpodo. We previously reported that AP-1 and Stratum regulate the trafficking of Notch and Sanpodo from the trans-Golgi network to the basolateral membrane. Loss of AP-1 or Stratum caused mild Notch gain-of-function phenotypes. Here, we report that their concomitant loss results in a penetrant Notch gain-of-function phenotype indicating that they control parallel pathways. While unequal partitioning of cell fate determinants and cell polarity were unaffected, we observed increased amounts of signaling-competent Notch as well as Delta and Sanpodo at the apical pIIa-pIIb interface at the expense of the basal pool of Notch. We propose that AP-1 and Stratum operate in parallel pathways to localize Notch and control where receptor activation takes place.