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Kinase-independent function of cyclin E

  1. Author:
    Geng, Y.
    Lee, Y. M.
    Welcker, M.
    Swanger, J.
    Zagozdzon, A.
    Winer, J. D.
    Roberts, J. M.
    Kaldis, P.
    Clurman, B. E.
    Sicinski, P.

  2. Author Address

    Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA. Fred Hutchinson Canc Res Ctr, Div Human Biol, Seattle, WA 98109 USA. Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98109 USA. Fred Hutchinson Canc Res Ctr, Howard Hughes Med Inst, Seattle, WA 98109 USA. Harvard Univ, Sch Med, Dept Canc Biol, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA. NCI, Mouse Canc Genet Program, Frederick, MD 21702 USA.;Clurman, BE, Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA.;bclurman@fhcrc.org peter_sicinski@dfci.harvard.edu
    1. Year: 2007
    2. Date: Jan
  2. Journal: Molecular Cell
    1. 25
    2. 1
    3. Pages: 127-139
  4. Type of Article: Article
  5. ISSN: 1097-2765
  1. Abstract:

    E-type cyclins are thought to drive cell-cycle progression by activating cyclin-dependent kinases, primarily CDK2. We previously found that cyclin E-null cells failed to incorporate MCM helicase into DNA prereplication complex during G(0) -> S phase progression. We now report that a kinase-deficient cyclin E mutant can partially restore MCM loading and S phase entry in cyclin E-null cells. We found that cyclin E is loaded onto chromatin during G(0) -> S progression. In the absence of cyclin E, CDT1 is normally loaded onto chromatin, whereas MCM is not, indicating that cyclin E acts between CDT1 and MCM loading. We observed a physical association of cyclin E with CDT1 and with MCMs. We propose that cyclin E facilitates MCM loading in a kinase-independent fashion, through physical interaction with CDT1 and MCM. Our work indicates that-in addition to their function as CDK activators-E cyclins play kinase-independent functions in cell-cycle progression.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000243566700010

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