Journal
DEVELOPMENTAL CELL
Volume 4, Issue 5, Pages 741-752Publisher
CELL PRESS
DOI: 10.1016/S1534-5807(03)00119-9
Keywords
-
Categories
Funding
- NIGMS NIH HHS [GM47238] Funding Source: Medline
Ask authors/readers for more resources
The cell division cycle requires oscillations in activity of B-type cyclin (Clb)-Cdk1 kinases. Oscillations are due to periodic cyclin degradation by the anaphase-promoting complex (APC) activated by Cdc20 or Cdh1, and to cyclical accumulation of the Sic1 inhibitor. The results presented here suggest that the regulatory machinery controlling Clb kinase levels embeds two distinct oscillatory mechanisms. One, a relaxation oscillator, involves alternation between two meta-stable states: Clb high/inhibitors (Sic1/APC-Cdh1) low, and Clb low/inhibitors high. The other, a negative feedback oscillator, involves Clb kinase activation of APC-Cdc20, leading to Clb degradation. Genetic analysis suggests that these two mechanisms can function independently, and inactivation of both mechanisms is required to prevent mitosis. Computational modeling confirms that two such mechanisms can be linked to yield a robust cell cycle control system.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available