Abstract：
:APPL1- and RAB5-positive signaling endosomes play a crucial role in the activation of AKT in response to extracellular stimuli. Myosin VI (MYO6) and two of its cargo adaptor proteins, GIPC and TOM1/TOM1L2, localize to these peripheral endosomes and mediate endosome association with cortical actin filaments. Loss of MYO6 leads to the displacement of these endosomes from the cell cortex and accumulation in the perinuclear space. Depletion of this myosin not only affects endosome positioning, but also induces actin and lipid remodeling consistent with endosome maturation, including accumulation of F-actin and the endosomal lipid PI(3)P. These processes acutely perturb endosome function, as both AKT phosphorylation and RAC-dependent membrane ruffling were markedly reduced by depletion of either APPL1 or MYO6. These results place MYO6 and its binding partners at a central nexus in cellular signaling linking actin dynamics at the cell surface and endosomal signaling in the cell cortex.
journal_name
Cell Repjournal_title
Cell reportsauthors
Masters TA,Tumbarello DA,Chibalina MV,Buss Fdoi
10.1016/j.celrep.2017.05.048subject
Has Abstractpub_date
2017-06-06 00:00:00pages
2088-2101issue
10issn
2211-1247pii
S2211-1247(17)30705-2journal_volume
19pub_type
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