The type V myosin-containing complex HUM is a RAB11 effector powering movement of secretory vesicles.

iScience

Department of Cellular and Molecular Biology, Centro de Investigaciones Biológicas CSIC, Ramiro de Maeztu 9, 28040 Madrid, Spain.

Published: July 2022

AI Article Synopsis

  • Kinesin-1/KinA transports secretory vesicles (SVs) to the hyphal tip, where they are taken over by type V myosin MyoE for concentration underneath the plasma membrane.
  • The stable HUM complex (HMSV-UDS1-MyoE) formed by RAB11 effector UDS1 and HMSV facilitates the interaction between RAB11-GTP and MyoE, crucial for the movement of SVs.
  • Disruption of UDS1 or HMSV leads to impaired transport of SVs to the apex, causing the dispersion of RAB11 SVs on the apical surface, indicating the reliance on KinA/microtubule transport mechanisms.

Article Abstract

In the apex-directed RAB11 exocytic pathway of , kinesin-1/KinA conveys secretory vesicles (SVs) to the hyphal tip, where they are transferred to the type V myosin MyoE. MyoE concentrates SVs at an apical store located underneath the PM resembling the presynaptic active zone. A rod-shaped RAB11 effector, UDS1, and the intrinsically disordered and coiled-coil HMSV associate with MyoE in a stable HUM (HMSV-UDS1-MyoE) complex recruited by RAB11 to SVs through an interaction network involving RAB11 and HUM components, with the MyoE globular tail domain (GTD) binding both HMSV and RAB11-GTP and RAB11-GTP binding both the MyoE-GTD and UDS1. UDS1 bridges RAB11-GTP to HMSV, an avid interactor of the MyoE-GTD. The interaction between the UDS1-HMSV sub-complex and RAB11-GTP can be reconstituted . Ablating UDS1 or HMSV impairs actomyosin-mediated transport of SVs to the apex, resulting in spreading of RAB11 SVs across the apical dome as KinA/microtubule-dependent transport gains prominence.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9213775PMC
http://dx.doi.org/10.1016/j.isci.2022.104514DOI Listing

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