Alphaherpesviral US3 kinase induces cofilin dephosphorylation to reorganize the actin cytoskeleton

J Virol. 2013 Apr;87(7):4121-6. doi: 10.1128/JVI.03107-12. Epub 2013 Jan 30.

Abstract

The conserved alphaherpesviral serine/threonine kinase US3 causes dramatic actin rearrangements, associated with increased viral spread. Here, we show that US3 of pseudorabies virus (PRV) leads to activation (dephosphorylation) of the central actin regulator cofilin. A mutation that impairs US3 kinase activity and the group I p21-activated kinase inhibitor IPA-3 inhibited US3-mediated cofilin activation. Additionally, expression of phosphomimetic S3D cofilin significantly suppressed the ability of US3 to cause cell projections and cell rounding. In conclusion, the US3 kinase of PRV leads to activation (dephosphorylation) of cofilin, and cofilin contributes to US3-mediated actin rearrangements.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actin Cytoskeleton / metabolism*
  • Actin Depolymerizing Factors / metabolism*
  • Blotting, Western
  • Cell Shape / physiology
  • Enzyme Inhibitors / metabolism
  • Herpesvirus 1, Suid / enzymology*
  • Microscopy, Fluorescence
  • Mutation
  • Phosphorylation
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Virus Internalization*
  • p21-Activated Kinases / antagonists & inhibitors

Substances

  • Actin Depolymerizing Factors
  • Enzyme Inhibitors
  • Protein Serine-Threonine Kinases
  • p21-Activated Kinases