Theoretical dynamics of the cyclin B-MPF system: a possible role for p13suc1

C D Thron1

  • 1Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, NH 03755-3835.

Bio Systems
|January 1, 1994
PubMed

Insights

The suc1 gene product p13 enhances cell division oscillations by inhibiting maturation promoting factor (MPF) activation. This inhibition is crucial for regulating MPF pulses, ensuring proper mitosis progression and cyclin degradation.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Mathematical Modeling

Background:

  • Cell division is regulated by maturation promoting factor (MPF), a complex of p34cdc2 and cyclin B.
  • MPF activation is autocatalytic and can lead to oscillations, potentially causing repeated mitosis.

Purpose of the Study:

  • To investigate the role of cofactors in regulating MPF-mediated cell cycle oscillations.
  • To mathematically model the effect of p13suc1 on MPF activation and its impact on mitosis.

Main Methods:

  • Mathematical analysis of a biochemical system involving MPF, p34cdc2, cyclin B, and p13suc1.
  • Modeling the autocatalytic activation of MPF and the influence of inhibitory cofactors.

Main Results:

  • p13suc1 acts as a cofactor that enhances oscillatory tendencies by inhibiting MPF autocatalytic action.
  • p13suc1 titration by MPF determines the threshold for MPF activation, creating a precursor backlog and a high reaction order for MPF autocatalysis.
  • This mechanism promotes autonomous oscillations and enhances system excitability, contributing to proper M phase progression.

Conclusions:

  • The p13suc1 cofactor plays a critical role in regulating MPF pulses, essential for triggering M phase events and subsequent cyclin degradation.
  • The model explains the seemingly paradoxical necessity of p13suc1 for mitosis, despite its inhibitory effect on MPF activation.

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