These F-actin and microtubules structurally support cells and provide the tracks on which cargo is transported within them ( 1). Thus, we identify a mechanism that spatiotemporally propagates F-actin disassembly while also proposing that other F-actin-trafficked-cargo is derailed by this disassembly to directionally orient rebuilding.Ĭells and tissue systems are built and remodeled through the ability of actin and tubulin proteins to associate and form long polymers, actin filaments (F-actin), and microtubules, respectively. Myo15’s broadening of Mical’s distribution also expands and directionally orients Mical-mediated F-actin disassembly and subsequent cellular remodeling, including in response to Semaphorin/Plexin cell surface activation signals. Myo15 specifically positions this F-actin disassembly by associating with Mical and using its motor and MyTH4-FERM cargo-transporting functions to broaden Mical’s distribution. Specifically, while unconventional myosins have been associated with transporting cargo along F-actin to spatially target cytoskeletal assembly, we now find they also target disassembly. Here, we identify that the unconventional class XV myosin physically and functionally interacts with the F-actin disassembly enzyme Mical to spatiotemporally position cellular breakdown and reconstruction. However, how F-actin-based changes occur with spatiotemporal precision and specific directional orientation is poorly understood. The F-actin cytoskeleton drives cellular form and function.
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