A new link between the c-Abl tyrosine kinase and phosphoinositide signalling through PLC-gamma1

Nat Cell Biol. 2003 Apr;5(4):309-19. doi: 10.1038/ncb949.

Abstract

The c-Abl tyrosine (Tyr) kinase is activated after platelet-derived-growth factor receptor (PDGFR) stimulation in a manner that is partially dependent on Src kinase activity. However, the activity of Src kinases alone is not sufficient for activation of c-Abl by PDGFR. Here we show that functional phospholipase C-gamma1 (PLC-gamma1) is required for c-Abl activation by PDGFR. Decreasing cellular levels of phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) by PLC-gamma1-mediated hydrolysis or dephosphorylation by an inositol polyphosphate 5-phosphatase (Inp54) results in increased Abl kinase activity. c-Abl functions downstream of PLC-gamma1, as expression of kinase-inactive c-Abl blocks PLC-gamma1-induced chemotaxis towards PDGF-BB. PLC-gamma1 and c-Abl form a complex in cells that is enhanced by PDGF stimulation. After activation, c-Abl phosphorylates PLC-gamma1 and negatively modulates its function in vivo. These findings uncover a newly discovered functional interdependence between non-receptor Tyr kinase and lipid signalling pathways.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Binding Sites / genetics
  • Cells, Cultured
  • Chemotaxis / genetics
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology
  • Eukaryotic Cells / enzymology*
  • Gene Expression Regulation, Enzymologic / physiology
  • Mutation / physiology
  • Phosphatidylinositol 4,5-Diphosphate / genetics
  • Phosphatidylinositol 4,5-Diphosphate / metabolism*
  • Phospholipase C gamma
  • Phosphorylation
  • Platelet-Derived Growth Factor / genetics
  • Platelet-Derived Growth Factor / metabolism*
  • Protein Structure, Tertiary / genetics
  • Proto-Oncogene Proteins c-abl / genetics
  • Proto-Oncogene Proteins c-abl / metabolism*
  • Receptor, Platelet-Derived Growth Factor beta / genetics
  • Receptor, Platelet-Derived Growth Factor beta / metabolism*
  • Recombinant Fusion Proteins / genetics
  • Signal Transduction / physiology*
  • Type C Phospholipases / antagonists & inhibitors
  • Type C Phospholipases / deficiency*
  • Type C Phospholipases / genetics

Substances

  • Enzyme Inhibitors
  • Phosphatidylinositol 4,5-Diphosphate
  • Platelet-Derived Growth Factor
  • Recombinant Fusion Proteins
  • Receptor, Platelet-Derived Growth Factor beta
  • Proto-Oncogene Proteins c-abl
  • Type C Phospholipases
  • Phospholipase C gamma