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Vol. 14, Issue 11, 4695-4706, November 2003
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Center for Biomedical Imaging Technology, Department of Physiology, University of Connecticut Health Center, Farmington, Connecticut 06032
Submitted April 21, 2003;
Revised June 29, 2003;
Accepted July 3, 2003
Monitoring Editor: Mark Solomon
During the cell cycle, Cdc2-cyclin B kinase abruptly becomes active and triggers the entry into mitosis/meiosis. Recently, it was found that inactive Cdc2-cyclin B is present in aggregates in immature starfish oocytes and becomes disaggregated at the time of its activation during maturation. We discuss a possible scenario in which aggregation of Cdc2-cyclin B dramatically enhances robustness of this activation. In this scenario, only inactive Cdc2-cyclin B can form aggregates, and the aggregates are in equilibrium with inactive Cdc2-cyclin B in solution. During maturation, the hormone-triggered inactivation of Myt1 depletes the soluble inactive Cdc2-cyclin B and the turnover leads to dissolution of the aggregates. This phase change, when coupled with the instability of the signaling network, provides a robust bio-switch.
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