Drosophila Cip4 and WASp define a branch of the Cdc42-Par6-aPKC pathway regulating E-Cadherin endocytosis

• Verfasst von: Leibfried, Andrea [VerfasserIn]
• Verfasst von: Fricke, Robert Patrick [VerfasserIn]
• Verfasst von: Morgan, Matthew J. [VerfasserIn]
• Verfasst von: Bogdan, Sven [VerfasserIn]
• Verfasst von: Bellaïche, Yohanns [VerfasserIn]
• Titel: Drosophila Cip4 and WASp define a branch of the Cdc42-Par6-aPKC pathway regulating E-Cadherin endocytosis
• Verf.angabe: Andrea Leibfried, Robert Fricke, Matthew J. Morgan, Sven Bogdan, and Yohanns Bellaiche
• E-Jahr: 2008
• Jahr: November 2008
• Umfang: 10 S.
• Fussnoten: Gesehen am 08.05.2023
• Titel Quelle: Enthalten in: Current biology
• Ort Quelle: London : Current Biology Ltd., 1991
• Jahr Quelle: 2008
• Band/Heft Quelle: 18(2008), 21 vom: Nov., Seite 1639-1648
• ISSN Quelle: 1879-0445
• DOI: doi:10.1016/j.cub.2008.09.063
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: CELLBIO
• Sach-SW: DEVBIO
• K10plus-PPN: 1844751155

Abstract

Background - Integral to the function and morphology of the epithelium is the lattice of cell-cell junctions known as adherens junctions (AJs). AJ stability and plasticity relies on E-Cadherin exocytosis and endocytosis. A mechanism regulating E-Cadherin (E-Cad) exocytosis to the AJs has implicated proteins of the exocyst complex, but mechanisms regulating E-Cad endocytosis from the AJs remain less well understood. - Results - Here we show that Cdc42, Par6, or aPKC loss of function is accompanied by the accumulation of apical E-Cad intracellular punctate structures and the disruption of AJs in Drosophila epithelial cells. These punctate structures derive from large and malformed endocytic vesicles that emanate from the AJs; a phenotype that is also observed upon blocking vesicle scission in dynamin mutant cells. We demonstrate that the Drosophila Cdc42-interacting protein 4 (Cip4) is a Cdc42 effector that interacts with Dynamin and the Arp2/3 activator WASp in Drosophila. Accordingly, Cip4, WASp, or Arp2/3 loss of function also results in defective E-Cadherin endocytosis. - Conclusion - Altogether our results show that Cdc42 functions with Par6 and aPKC to regulate E-Cad endocytosis and define Cip4 and WASp as regulators of the early E-Cad endocytic events in epithelial tissue.