The Clathrin adaptor AP-1 and Stratum act in parallel pathways to control Notch activation in Drosophila sensory organ precursors cells

sensory organ precursors divide asymmetrically to generate pIIa/pIIb cells, the identity of which relies on activation of Notch at cytokinesis. Although 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 contri...

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Published in:Development (Cambridge) Vol. 148; no. 1
Main Authors: Bellec, Karen, Pinot, Mathieu, Gicquel, Isabelle, Le Borgne, Roland
Format: Journal Article
Language:English
Published: England The Company of Biologists Ltd 10-01-2021
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Summary:sensory organ precursors divide asymmetrically to generate pIIa/pIIb cells, the identity of which relies on activation of Notch at cytokinesis. Although 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 signalling requires appropriate apico-basal targeting of Notch, its ligand Delta and its trafficking partner Sanpodo. We have previously reported that AP-1 and Stratum regulate the trafficking of Notch and Sanpodo from the -Golgi network to the basolateral membrane. Loss of AP-1 or Stratum caused mild gain-of-function phenotypes. Here, we report that their concomitant loss results in a penetrant gain-of-function phenotype, indicating that they control parallel pathways. Although unequal partitioning of cell fate determinants and cell polarity were unaffected, we observed increased amounts of signalling-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.
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Equipe Labellisée Ligue Nationale contre le cancer
Handling Editor: François Guillemot
Present address: Wolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1QH, UK.
ISSN:1477-9129
0950-1991
1477-9129
DOI:10.1242/dev.191437