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A virtual cycle: theory and experiment converge on the exit from mitosis
F1000 Biology Reports
|October 16, 2010
Summary
The cell division cycle relies on cyclin-dependent kinase (CDK) activity thresholds. Systems-level control ensures unidirectional progression through mitosis and DNA replication.
Area of Science:
- Cell biology
- Molecular biology
- Biophysics
Background:
- The cell division cycle is regulated by cyclin-dependent kinase (CDK) activity.
- CDK activity thresholds govern DNA synthesis and entry into mitosis.
- Mitotic exit and replication origin re-setting occur when CDK activity falls below thresholds.
Purpose of the Study:
- To model the cell division cycle based on CDK activity thresholds.
- To investigate the mechanisms ensuring unidirectional cell cycle progression.
- To understand the role of systems-level control in regulating CDK and phosphatase activities during mitotic exit.
Main Methods:
- Computational modeling of the cell division cycle.
- Experimental analysis of mitotic exit.
- Quantitative assessment of CDK and phosphatase activities.
Main Results:
- A simple rise and fall of CDK activity may suffice for alternating chromosome duplication and segregation.
- Experimental data suggest a more complex mechanism for mitotic exit.
- Systems-level control of CDK function and the balance between CDK and phosphatase activities ensure unidirectional progression.
Conclusions:
- The cell division cycle is governed by quantitative thresholds of CDK activity.
- Mitotic exit involves complex systems-level regulation beyond simple CDK activity collapse.
- Maintaining the balance between mitotic CDK and phosphatase activities is crucial for cell cycle progression.
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