Role of the PI3K regulatory subunit in the control of actin organization and cell migration

J Cell Biol. 2000 Oct 16;151(2):249-62. doi: 10.1083/jcb.151.2.249.

Abstract

Cell migration represents an important cellular response that utilizes cytoskeletal reorganization as its driving force. Here, we describe a new signaling cascade linking PDGF receptor stimulation to actin rearrangements and cell migration. We demonstrate that PDGF activates Cdc42 and its downstream effector N-WASP to mediate filopodia formation, actin stress fiber disassembly, and a reduction in focal adhesion complexes. Induction of the Cdc42 pathway is independent of phosphoinositide 3-kinase (PI3K) enzymatic activity, but it is dependent on the p85alpha regulatory subunit of PI3K. Finally, data are provided showing that activation of this pathway is required for PDGF-induced cell migration on collagen. These observations show the essential role of the PI3K regulatory subunit p85alpha in controlling PDGF receptor-induced cytoskeletal changes and cell migration, illustrating a novel signaling pathway that links receptor stimulation at the cell membrane with actin dynamics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3 Cells
  • Actin Cytoskeleton
  • Actins / metabolism*
  • Animals
  • Cell Adhesion
  • Cell Movement*
  • Fluorescent Antibody Technique
  • Mice
  • Microscopy, Video
  • Models, Biological
  • Nerve Tissue Proteins / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Protein Subunits
  • Pseudopodia
  • Receptors, Platelet-Derived Growth Factor / metabolism*
  • Signal Transduction
  • Stress Fibers / metabolism*
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • cdc42 GTP-Binding Protein / metabolism

Substances

  • Actins
  • Nerve Tissue Proteins
  • Protein Subunits
  • Wasl protein, mouse
  • Wiskott-Aldrich Syndrome Protein, Neuronal
  • Phosphatidylinositol 3-Kinases
  • Receptors, Platelet-Derived Growth Factor
  • cdc42 GTP-Binding Protein