Substrate rigidity and force define form through tyrosine phosphatase and kinase pathways

Trends Cell Biol. 2006 Apr;16(4):213-23. doi: 10.1016/j.tcb.2006.02.005. Epub 2006 Mar 10.


Cell forces define cell morphology, alterations in which are caused by tyrosine kinase and phosphatase mutations, which implies a causal linkage. Recent studies have shown that phosphotyrosine signaling is involved in force sensing for cells on flat surfaces. Early force-dependent activation of Src family kinases by phosphatases or cytoskeleton stretch leads to the activation of downstream signaling. In addition, force generation by cells depends on a feedback mechanism between matrix rigidity or force generation and myosin contractility. Components of the force-sensing pathway are linked to the integrin-cytoskeleton complex at sites of force application and serve as scaffolds for signaling processes. Thus, early events in force detection are mechanically induced cytoskeletal changes that result in biochemical signals to mechanoresponsive pathways that then regulate cell form.

Publication types

  • Review

MeSH terms

  • Adherens Junctions / metabolism*
  • Animals
  • Cell Adhesion
  • Cell Movement
  • Cytoskeleton / metabolism
  • Enzyme Activation
  • Humans
  • Mechanotransduction, Cellular*
  • Models, Biological
  • Muscle Rigidity
  • Protein Tyrosine Phosphatases / metabolism
  • Protein Tyrosine Phosphatases / physiology*
  • Protein-Tyrosine Kinases / metabolism
  • Protein-Tyrosine Kinases / physiology*
  • Signal Transduction*
  • Substrate Specificity


  • Protein-Tyrosine Kinases
  • Protein Tyrosine Phosphatases