MYO1C stabilizes actin and facilitates arrival of transport carriers at the Golgi apparatus

Nom de la revue
Journal of Cell Science
Anahi Capmany, Azumi Yoshimura, Rachid Kerdous, Valentina Caorsi, Aurianne Lescure, Elaine Del Nery, Evelyne Coudrier, Bruno Goud, Kristine Schauer

We aim to identify the myosin motor proteins that control trafficking at the Golgi apparatus. In addition to the known Golgi-associated myosins MYO6, MYO18A and MYH9 (myosin IIA), we identify MYO1C as a novel player at the Golgi. We demonstrate that depletion of MYO1C induces Golgi apparatus fragmentation and decompaction. MYO1C accumulates at dynamic structures around the Golgi apparatus that colocalize with Golgi-associated actin dots. MYO1C depletion leads to loss of cellular F-actin, and Golgi apparatus decompaction is also observed after the inhibition or loss of the Arp2/3 complex. We show that the functional consequences 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 apparatus facilitating the arrival of incoming transport carriers at the Golgi.