ER contact sites define the position of endosome bud fission during actin-dependent cargo sorting. Disrupting endosomal actin structures prevents retrograde cargo movement; however, how actin a↵ects ER contact site formation and endosome fission is not known. Here I show that in contrast with the WASH complex, actin, its nucleator ARP2/3, and COR1C form a contained structure at the bud neck that defines the site of bud fission. I find that actin confinement is facilitated by Type I coronins. Depletion of Type I coronins, allows actin to extend along the length of the bud in an ARP2/3 dependent manner. I demonstrate that extension of branched actin prevents ER recruitment and stalls buds prior to fission. Finally, my structure-function studies show that the COR1C’s coiled-coil domain is sucient to restore actin confinement, ER recruitment, and endosome fission. Together my data reveal how the dynamics of endosomal actin and activity of actin regulators organize ER-associated bud fission
