Light-dependent inhibition of clathrin-mediated endocytosis in yeast unveils conserved functions of the AP2 complex

[EN] Clathrin-mediated endocytosis (CME) is an essential cellular process, conserved among eukaryotes. Yeast constitutes a powerful genetic model to dissect the complex endocytic machinery, yet there is a lack of specific pharmacological agents to interfere with CME in these organisms. TL2 is a ligh...

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Detalles Bibliográficos
Autores: Prischich, Davia, Camarero, Núria, Encinar del Dedo, Javier, Cambra Pellejà, Maria, Prat, Judit, Nevola, Laura, Martín Quirós, Andrés, Rebollo, Elena, Pastor, Laura, Giralt, Ernest, Geli, María Isabel, Gorostiza, Pau
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Institución:Universidad de León
Repositorio:BULERIA. Repositorio Institucional de la Universidad de León
OAI Identifier:oai:buleria.unileon.es:10612/18589
Acceso en línea:https://www.sciencedirect.com/science/article/pii/S2589004223019764?via%3Dihub
https://hdl.handle.net/10612/18589
Access Level:acceso abierto
Palabra clave:Sanidad animal
Endocytosis
AP2 complex
3109 Ciencias Veterinarias
Descripción
Sumario:[EN] Clathrin-mediated endocytosis (CME) is an essential cellular process, conserved among eukaryotes. Yeast constitutes a powerful genetic model to dissect the complex endocytic machinery, yet there is a lack of specific pharmacological agents to interfere with CME in these organisms. TL2 is a light-regulated peptide inhibitor targeting the AP2-β-adaptin/β-arrestin interaction and that can photocontrol CME with high spatiotemporal precision in mammalian cells. Here, we study endocytic protein dynamics by live-cell imaging of the fluorescently tagged coat-associated protein Sla1-GFP, demonstrating that TL2 retains its inhibitory activity in S. cerevisiae spheroplasts. This is despite the β-adaptin/β-arrestin interaction not being conserved in yeast. Our data indicate that the AP2 α-adaptin is the functional target of activated TL2. We identified as interacting partners for the α-appendage, the Eps15 and epsin homologues Ede1 and Ent1. This demonstrates that endocytic cargo loading and sensing can be executed by conserved molecular interfaces, regardless of the proteins involved