期刊
MOLECULAR BIOLOGY OF THE CELL
卷 14, 期 11, 页码 4695-4706出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E03-04-0248
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- NCRR NIH HHS [P41 RR013186, RR-13186] Funding Source: Medline
- NIGMS NIH HHS [R01-GM60389, R01 GM060389] Funding Source: Medline
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR013186] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM060389] Funding Source: NIH RePORTER
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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