The control of cell motility and epithelial morphogenesis by Jun kinases

Trends Cell Biol. 2004 Feb;14(2):94-101. doi: 10.1016/j.tcb.2003.12.005.


Originally identified as stress-activated protein kinases that control cell survival and proliferation through transcription factor c-Jun, the Jun N-terminal kinase (JNK) subgroup of MAP kinases (MAPKs) have recently emerged as crucial regulators of cell migration and the morphogenetic movement of epithelial sheets. In Drosophila, a well-orchestrated JNK signaling pathway controls formation of actin stress fibers and cell shape changes, which are required for the sealing of embryonic epidermis in a process known as dorsal closure. The JNK pathway is also involved in morphogenetic processes in mice including closure of the eyelid, neural tube and optic fissure. This article focuses on recent advances in understanding the role of JNK pathway in the regulation of cell migration, cytoskeleton rearrangement and the morphogenesis of epithelial sheets.

Publication types

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

MeSH terms

  • Animals
  • Body Patterning / physiology
  • Cell Differentiation / physiology
  • Cell Movement / physiology*
  • Cytoskeleton / metabolism
  • Embryo, Mammalian / cytology
  • Embryo, Mammalian / embryology
  • Embryo, Mammalian / metabolism
  • Epithelial Cells / cytology
  • Epithelial Cells / enzymology*
  • Epithelium / enzymology
  • Epithelium / growth & development*
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases / metabolism*
  • Organogenesis / physiology*


  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases