Microtubule plus-ends act as physical signaling hubs to activate RhoA during cytokinesis

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Abstract

Microtubules (MTs) are essential for cleavage furrow positioning during cytokinesis, but the mechanisms by which MT-derived signals spatially define regions of cortical contractility are unresolved. In this study cytokinesis regulators visualized in Drosophila melanogaster (Dm) cells were found to localize to and track MT plus-ends during cytokinesis. The RhoA GEF Pebble (Dm ECT2) did not evidently tip-track, but rather localized rapidly to cortical sites contacted by MT plus-tips, resulting in RhoA activation and enrichment of myosin-regulatory light chain. The MT plus-end localization of centralspindlin was compromised following EB1 depletion, which resulted in a higher incidence of cytokinesis failure. Centralspindlin plus-tip localization depended on the C-terminus and a putative EB1-interaction motif (hxxPTxh) in RacGAP50C. We propose that MT plus-end-associated centralspindlin recruits a cortical pool of Dm ECT2 upon physical contact to activate RhoA and to trigger localized contractility.

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All data generated or analysed during this study are included in the manuscript and supporting files.

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Vikash Verma

Biology Department, University of Massachusetts, Amherst, Amherst, United States

Competing interests
The authors declare that no competing interests exist.
Thomas J Maresca

Biology Department, University of Massachusetts, Amherst, Amherst, United States

For correspondence
tmaresca@bio.umass.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0003-2214-8674

Funding

National Institute of General Medical Sciences (GM107026)

Thomas J Maresca

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

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This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.