info:eu-repo/semantics/article
MYO1C stabilizes actin and facilitates the arrival of transport carriers at the Golgi complex
Fecha
2019-04Registro en:
Capmany, Anahi; Yoshimura, Azumi; Kerdous, Rachid; Caorsi, Valentina; Lescure, Aurianne; et al.; MYO1C stabilizes actin and facilitates the arrival of transport carriers at the Golgi complex; Company of Biologists; Journal of Cell Science; 132; 8; 4-2019; 1-46
0021-9533
1477-9137
CONICET Digital
CONICET
Autor
Capmany, Anahi
Yoshimura, Azumi
Kerdous, Rachid
Caorsi, Valentina
Lescure, Aurianne
Nery, Elaine Del
Coudrier, Evelyne
Goud, Bruno
Schauer, Kristine
Resumen
In this study, we aimed to identify the myosin motor proteins that control trafficking at the Golgi complex. In addition to the known Golgi-associated myosins MYO6, MYO18A and MYH9 (myosin IIA), we identified MYO1C as a novel player at the Golgi in a human cell line. We demonstrate that depletion of MYO1C induces Golgi complex fragmentation and decompaction. MYO1C accumulates at dynamic structures around the Golgi complex that colocalize with Golgi-associated actin dots. MYO1C depletion leads to loss of cellular F-actin, and Golgi complex decompaction is also observed after inhibition or loss of the actin-related protein 2/3 complex, Arp2/3 (also known as ARPC). We show that the functional consequence of MYO1C depletion is a delay in the arrival of incoming transport carriers, both from the anterograde and retrograde routes. We propose that MYO1C stabilizes actin at the Golgi complex, facilitating the arrival of incoming transport carriers at the Golgi.This article has an associated First Person interview with the first author of the paper.