Myotonic dystrophy protein kinase (DMPK) induces actin cytoskeletal reorganization and apoptotic-like blebbing in lens cells

Cell Motil Cytoskeleton. 2000 Feb;45(2):133-48. doi: 10.1002/(SICI)1097-0169(200002)45:2<133::AID-CM5>3.0.CO;2-S.


DMPK, the product of the DM locus, is a member of the same family of serine-threonine protein kinases as the Rho-associated enzymes. In DM, membrane inclusions accumulate in lens fiber cells producing cataracts. Overexpression of DMPK in cultured lens epithelial cells led to apoptotic-like blebbing of the plasma membrane and reorganization of the actin cytoskeleton. Enzymatically active DMPK was necessary for both effects; inactive mutant DMPK protein did not produce either effect. Active RhoA but not constitutive GDP-state mutant protein produced similar effects as DMPK. The similar actions of DMPK and RhoA suggest that they may function in the same regulatory network. The observed effects of DMPK may be relevant to the removal of membrane organelles during normal lens differentiation and the retention of intracellular membranes in DM lenses.

Publication types

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

MeSH terms

  • Actins / metabolism*
  • Apoptosis*
  • Cells, Cultured
  • Cytoskeleton / physiology*
  • Humans
  • Lens, Crystalline / metabolism*
  • Lens, Crystalline / pathology
  • Myotonic Dystrophy / enzymology
  • Myotonic Dystrophy / pathology
  • Myotonin-Protein Kinase
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / metabolism*
  • Transfection
  • rhoA GTP-Binding Protein / biosynthesis
  • rhoA GTP-Binding Protein / metabolism


  • Actins
  • DMPK protein, human
  • Myotonin-Protein Kinase
  • Protein-Serine-Threonine Kinases
  • rhoA GTP-Binding Protein