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Antagonistic forces generated by cytoplasmic dynein and myosin-II during growth cone turning and axonal retraction
Journal article   Open access

Antagonistic forces generated by cytoplasmic dynein and myosin-II during growth cone turning and axonal retraction

Kenneth A Myers, Irina Tint, C Vidya Nadar, Yan He, Mark M Black and Peter W Baas
Traffic (Copenhagen, Denmark), v 7(10), pp 1333-1351
Oct 2006
DOI: https://doi.org/10.1111/j.1600-0854.2006.00476.x
PMID: 16911591
Featured in Collection :   UN Sustainable Development Goals @ Drexel
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https://doi.org/10.1111/j.1600-0854.2006.00476.xView
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze),  Open

Abstract

Dyneins - metabolism Green Fluorescent Proteins - metabolism Microtubule-Associated Proteins - genetics Microtubule-Associated Proteins - metabolism Tubulin Modulators - pharmacology Actins - metabolism Fluorescent Dyes - metabolism Rats Cytoplasm - metabolism Neurons - cytology Axons - physiology Green Fluorescent Proteins - genetics Cell Movement - physiology Microtubules - metabolism Animals Growth Cones - metabolism Myosin Type II - metabolism Cell Shape Axons - ultrastructure Vinblastine - pharmacology Growth Cones - drug effects Laminin - metabolism Nitric Oxide - metabolism RNA, Small Interfering - metabolism
Cytoplasmic dynein transports short microtubules down the axon in part by pushing against the actin cytoskeleton. Recent studies have suggested that comparable dynein-driven forces may impinge upon the longer microtubules within the axon. Here, we examined a potential role for these forces on axonal retraction and growth cone turning in neurons partially depleted of dynein heavy chain (DHC) by small interfering RNA. While DHC-depleted axons grew at normal rates, they retracted far more robustly in response to donors of nitric oxide than control axons, and their growth cones failed to efficiently turn in response to substrate borders. Live cell imaging of dynamic microtubule tips showed that microtubules in DHC-depleted growth cones were largely confined to the central zone, with very few extending into filopodia. Even under conditions of suppressed microtubule dynamics, DHC depletion impaired the capacity of microtubules to advance into the peripheral zone of the growth cone, indicating a direct role for dynein-driven forces on the distribution of the microtubules. These effects were all reversed by inhibition of myosin-II forces, which are known to underlie the retrograde flow of actin in the growth cone and the contractility of the cortical actin during axonal retraction. Our results are consistent with a model whereby dynein-driven forces enable microtubules to overcome myosin-II-driven forces, both in the axonal shaft and within the growth cone. These dynein-driven forces oppose the tendency of the axon to retract and permit microtubules to advance into the peripheral zone of the growth cone so that they can invade filopodia.

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Collaboration types
Domestic collaboration
Web of Science research areas
Cell Biology
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