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Drosophila HOPS and AP-3 complex genes are required for a Deltex-regulated activation of notch in the endosomal trafficking pathway.

Abstract：

:DSL ligands promote proteolysis of the Notch receptor, to release active Notch intracellular domain (N(ICD)). Conversely, the E3 ubiquitin ligase Deltex can activate ligand-independent Notch proteolysis and signaling. Here we show that Deltex effects require endocytic trafficking by HOPS and AP-3 complexes. Our data suggest that Deltex shunts Notch into an endocytic pathway with two possible endpoints. If Notch transits into the lysosome lumen, it is degraded. However, if HOPS and AP-3 deliver Notch to the limiting membrane of the lysosome, degradation of the Notch extracellular domain allows subsequent Presenilin-mediated release of N(ICD). This model accounts for positive and negative regulatory effects of Deltex in vivo. Indeed, we uncover HOPS/AP-3 contributions to Notch signaling during Drosophila midline formation and neurogenesis. We discuss ways in which these endocytic pathways may modulate ligand-dependent and -independent events, as a mechanism that can potentiate Notch signaling or dampen noise in the signaling network.

journal_name

Dev Cell

journal_title

Developmental cell

authors

Wilkin M,Tongngok P,Gensch N,Clemence S,Motoki M,Yamada K,Hori K,Taniguchi-Kanai M,Franklin E,Matsuno K,Baron M

doi

10.1016/j.devcel.2008.09.002

subject

Has Abstract

pub_date

2008-11-01 00:00:00

pages

762-72

issue

5

eissn

1534-5807

issn

1878-1551

pii

S1534-5807(08)00371-7

journal_volume

15

pub_type

杂志文章

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