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Establishment of a Clinically Relevant Ex Vivo Mock Cataract Surgery Model for Investigating Epithelial Wound Repair in a Native Microenvironment
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Modeling the roles of protein kinase Cβ and η in single-cell wound repair

William R Holmes1, Laura Liao2, William Bement3

  • 1Department of Mathematics and Statistics, University of Melbourne, Melbourne, VIC 3010, Australia.

Molecular Biology of the Cell
|August 28, 2015
PubMed

Insights

Protein kinases PKCβ and PKCη regulate Rho GTPase patterning at wounded Xenopus oocyte cells. PKCβ enhances Rho feedback, while PKCη affects Cdc42 inactivation, explaining observed zone inversions.

Area of Science:

  • Cell biology
  • Biophysics
  • Biochemistry

Background:

  • Wounded Xenopus oocytes exhibit actin-myosin network assembly regulated by Rho GTPases (Rho, Cdc42).
  • Rho and Cdc42 display distinct spatial patterning around wounds: Rho forms an inner ring, Cdc42 an outer ring.
  • Protein Kinase C (PKC) isoforms, specifically PKCβ and PKCη, modulate Rho and Cdc42 activity.

Purpose of the Study:

  • To investigate the roles of PKCβ and PKCη in Rho GTPase patterning at cell wounds.
  • To understand the molecular mechanisms underlying the spatial regulation of Rho and Cdc42 by these kinases.

Main Methods:

  • Adaptation of a mathematical model by Simon and coworkers.
  • Computational simulation to probe kinase functions in Rho GTPase regulation.

Main Results:

  • PKCβ appears to influence the magnitude of positive Rho-Abr feedback.
  • PKCη is implicated in the inactivation of Cdc42.
  • The model successfully explains qualitative and quantitative aspects of PKC-Rho GTPase interactions.
  • The model accounts for zone inversions observed in cells overexpressing PKCη.

Conclusions:

  • PKCβ and PKCη play distinct regulatory roles in establishing Rho GTPase spatial patterns during wound healing.
  • Mathematical modeling provides insights into the complex interplay between kinases and GTPases in cellular response to damage.
  • The findings contribute to understanding cell mechanics and signaling pathways in wound repair.

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