Arp2/3 complex-deficient mouse fibroblasts are viable and have normal leading-edge actin structure and function

Proc Natl Acad Sci U S A. 2005 Nov 8;102(45):16263-8. doi: 10.1073/pnas.0508228102. Epub 2005 Oct 27.

Abstract

RNA interference silencing of up to 90% of Arp3 protein expression, a major subunit of the Arp2/3 complex, proportionately decreases the intracellular motility of Listeria monocytogenes and actin nucleation activity ascribable to the Arp2/3 complex in mouse embryonic fibroblasts. However, the Arp2/3-deficient cells exhibit unimpaired lamellipodial actin network structure, translational locomotion, spreading, actin assembly, and ruffling responses. In addition, Arp3-silenced cells expressing neural Wiskott-Aldrich syndrome protein-derived peptides that inhibit Arp2/3 complex function in wild-type cells retained normal PDGF-induced ruffling. The Arp2/3 complex can be dispensable for leading-edge actin remodeling.

MeSH terms

  • Actin-Related Protein 2-3 Complex / genetics
  • Actin-Related Protein 2-3 Complex / physiology*
  • Actins / chemistry*
  • Actins / physiology
  • Animals
  • Cells, Cultured
  • Fibroblasts / physiology
  • Gene Silencing
  • Mice
  • Platelet-Derived Growth Factor / pharmacology
  • RNA Interference

Substances

  • Actin-Related Protein 2-3 Complex
  • Actins
  • Platelet-Derived Growth Factor