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Myosin light chain kinase regulates cell polarization independently of membrane tension or Rho kinase.

Authors
  • Lou, Sunny S
  • Diz-Muñoz, Alba
  • Weiner, Orion D
  • Fletcher, Daniel A
  • Theriot, Julie A
Type
Published Article
Journal
Journal of Cell Biology
Publisher
Rockefeller University Press
Publication Date
Apr 27, 2015
Volume
209
Issue
2
Pages
275–288
Identifiers
DOI: 10.1083/jcb.201409001
PMID: 25918227
Source
Medline
License
Unknown

Abstract

Cells polarize to a single front and rear to achieve rapid actin-based motility, but the mechanisms preventing the formation of multiple fronts are unclear. We developed embryonic zebrafish keratocytes as a model system for investigating establishment of a single axis. We observed that, although keratocytes from 2 d postfertilization (dpf) embryos resembled canonical fan-shaped keratocytes, keratocytes from 4 dpf embryos often formed multiple protrusions despite unchanged membrane tension. Using genomic, genetic, and pharmacological approaches, we determined that the multiple-protrusion phenotype was primarily due to increased myosin light chain kinase (MLCK) expression. MLCK activity influences cell polarity by increasing myosin accumulation in lamellipodia, which locally decreases protrusion lifetime, limiting lamellipodial size and allowing for multiple protrusions to coexist within the context of membrane tension limiting protrusion globally. In contrast, Rho kinase (ROCK) regulates myosin accumulation at the cell rear and does not determine protrusion size. These results suggest a novel MLCK-specific mechanism for controlling cell polarity via regulation of myosin activity in protrusions.

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