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Tome-1, a trigger of mitotic entry, is degraded during G1 via the APC

  1. Author:
    Ayad, N. G.
    Rankin, S.
    Murakami, M.
    Jebanathirajah, J.
    Gygi, S.
    Kirschner, M. W.

  2. Author Address

    Harvard Univ, Sch Med, Dept Cell Biol, 200 Longwood Ave, Boston, MA 02115 USA Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA Harvard Univ, Sch Med, Taplin Biol Mass Spectrometry Facil, Boston, MA 02115 USA NCI, Frederick, MD 21702 USA Kirschner MW Harvard Univ, Sch Med, Dept Cell Biol, 200 Longwood Ave, Boston, MA 02115 USA
    1. Year: 2003
  2. Journal: Cell
    1. 113
    2. 1
    3. Pages: 101-113
  4. Type of Article: Article
  1. Abstract:

    Entry into mitosis requires the activation of cdk1/ cyclin B, while mitotic exit is achieved when the same kinase activity decreases, as cyclin B is degraded. Cyclin B proteolysis is mediated by the anaphase promoting complex, or APC, an E3 ligase that is active at anaphase in mitosis through G1. We have identified a G1 substrate of the APC that we have termed Tome-1, for trigger of mitotic entry. Tome-1 is a cytosolic protein required for proper activation of cdk1/cyclin B and mitotic entry. Tome-1 associates with Skp-1 and is required for degradation of the cdk1 inhibitory tyrosine kinase wee1; Tome-1 therefore appears to be acting as part of an SCF-type E3 for wee1. Degradation of Tome-1 during G1 allows for wee 1 accumulation during interphase, thereby providing a critical link between the APC and SCF pathways in regulation of cclk1/cyclin B activity and thus mitotic entry and exit.

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