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CKA, a novel multidomain protein, regulates the JUN N-terminal kinase signal transduction pathway in Drosophila

  1. Author:
    Chen, H. W.
    Marinissen, M. J.
    Oh, S. W.
    Chen, X.
    Melnick, M.
    Perrimon, N.
    Gutkind, J. S.
    Hou, S. X.
  2. Author Address

    NCI, FCRDC, Immunol Lab, NIH, Bldg 560, Room 12-70, Frederick, MD 21702 USA. NCI, FCRDC, Immunol Lab, NIH, Frederick, MD 21702 USA. New England Biolabs Inc, Lab Cell Signaling, Beverly, MA 01915 USA. Natl Inst Dent & Craniofacial Res, Oral & Pharyngeal Canc Branch, NIH, Bethesda, MD 20892 USA. Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Genet, Boston, MA 02115 USA. Hou SX NCI, FCRDC, Immunol Lab, NIH, Bldg 560, Room 12-70, Frederick, MD 21702 USA.
    1. Year: 2002
  1. Journal: Molecular and Cellular Biology
    1. 22
    2. 6
    3. Pages: 1792-1803
  2. Type of Article: Article
  1. Abstract:

    The Drosophila melanogaster JUN N-terminal kinase (DJNK) and DPP (decapentaplegic) signal transduction pathways coordinately regulate epithelial cell sheet movement during the process of dorsal closure in the embryo. By a genetic screen of mutations affecting dorsal closure in Drosophila, we have now identified a multidomain protein, connector of kinase to AP-1 (cka), that functions in the DJNK pathway and controls the localized expression of dpp in the leading-edge cells. We have also investigated how CKA acts. This unique molecule forms a complex with HEP (DJNKK), BSK (DJNK), DJUN, and DFOS. Complex formation activates BSK kinase, which in turn phosphorylates and activates DJUN and DFOS. These data suggest that CKA represents a novel molecule regulating AP-1 activity by organizing a molecular complex of kinases and transcription factors, thus coordinating the spatial-temporal expression of AP-1-regulated genes.

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