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 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 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.