Focal adhesion kinase is not required for integrin function or viability in Drosophila

Development. 2004 Dec;131(23):5795-805. doi: 10.1242/dev.01462. Epub 2004 Nov 3.


The mammalian focal adhesion kinase (FAK) family of non-receptor protein-tyrosine kinases has been implicated in controlling a multitude of cellular responses to the engagement of cell-surface integrins and G-protein-coupled receptors. The high level of sequence conservation between the mammalian proteins and the Drosophila homologue of FAK, Fak56, suggested that it would have similar functions. However, we show here that Drosophila Fak56 is not essential for integrin functions in adhesion, migration or signaling in vivo. Furthermore, animals lacking Fak56 are viable and fertile, demonstrating that Fak56 is not essential for other developmental or physiological functions. Despite this, overexpressed Fak56 is a potent inhibitor of integrins binding to the extracellular matrix, suggesting that Fak56 may play a subtle role in the negative regulation of integrin adhesion.

Publication types

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

MeSH terms

  • Animals
  • Blotting, Southern
  • Blotting, Western
  • Cell Membrane / metabolism
  • Cytoskeleton / metabolism
  • DNA / metabolism
  • Down-Regulation
  • Drosophila
  • Drosophila Proteins
  • Drosophila melanogaster
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases
  • Gene Deletion
  • Gene Expression Regulation*
  • Immunoblotting
  • Integrins / metabolism*
  • Models, Genetic
  • Muscles / embryology
  • Mutation
  • Phenotype
  • Phosphorylation
  • Protein Structure, Tertiary
  • Protein-Tyrosine Kinases / genetics*
  • Protein-Tyrosine Kinases / physiology*
  • Signal Transduction
  • Transgenes
  • Tyrosine / metabolism


  • Drosophila Proteins
  • Integrins
  • Tyrosine
  • DNA
  • Protein-Tyrosine Kinases
  • Fak protein, Drosophila
  • Focal Adhesion Kinase 1
  • Focal Adhesion Protein-Tyrosine Kinases