public model
Short description
Gardner1998 - Cell Cycle Goldbeter

Mathematical modeling of cell division cycle (CDC) dynamics.

The SBML file has been generated by MathSBML 2.6.0.p960929 (Prerelease Version of 29-Sept-2006) 1-October-2006 15:36:36.076517.

This model is described in the article:

Gardner TS, Dolnik M, Collins JJ.
Proc. Natl. Acad. Sci. U.S.A. 1998 Nov; 95(24): 14190-14195

Abstract:

We demonstrate, by using mathematical modeling of cell division cycle (CDC) dynamics, a potential mechanism for precisely controlling the frequency of cell division and regulating the size of a dividing cell. Control of the cell cycle is achieved by artificially expressing a protein that reversibly binds and inactivates any one of the CDC proteins. In the simplest case, such as the checkpoint-free situation encountered in early amphibian embryos, the frequency of CDC oscillations can be increased or decreased by regulating the rate of synthesis, the binding rate, or the equilibrium constant of the binding protein. In a more complex model of cell division, where size-control checkpoints are included, we show that the same reversible binding reaction can alter the mean cell mass in a continuously dividing cell. Because this control scheme is general and requires only the expression of a single protein, it provides a practical means for tuning the characteristics of the cell cycle in vivo.

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Format
SBML (L2V4)
Related Publication
  • A theory for controlling cell cycle dynamics using a reversibly binding inhibitor.
  • Gardner TS, Dolnik M, Collins JJ
  • Proceedings of the National Academy of Sciences of the United States of America , 11/ 1998 , Volume 95 , pages: 14190-14195
  • Center for BioDynamics and Department of Biomedical Engineering, Boston University, 44 Cummington Street, Boston, MA 02215, USA.
  • We demonstrate, by using mathematical modeling of cell division cycle (CDC) dynamics, a potential mechanism for precisely controlling the frequency of cell division and regulating the size of a dividing cell. Control of the cell cycle is achieved by artificially expressing a protein that reversibly binds and inactivates any one of the CDC proteins. In the simplest case, such as the checkpoint-free situation encountered in early amphibian embryos, the frequency of CDC oscillations can be increased or decreased by regulating the rate of synthesis, the binding rate, or the equilibrium constant of the binding protein. In a more complex model of cell division, where size-control checkpoints are included, we show that the same reversible binding reaction can alter the mean cell mass in a continuously dividing cell. Because this control scheme is general and requires only the expression of a single protein, it provides a practical means for tuning the characteristics of the cell cycle in vivo.
Contributors
Nicolas Le Novère

Metadata information

isDerivedFrom
BioModels Database BIOMD0000000003
BioModels Database BIOMD0000000004
is
BioModels Database MODEL6614879888
BioModels Database BIOMD0000000008
isDescribedBy
PubMed 9826676
hasTaxon
Taxonomy Xenopus laevis
isVersionOf
Gene Ontology mitotic cell cycle
isHomologTo
Curation status
Curated
  • Model originally submitted by : Nicolas Le Novère
  • Submitted: Sep 13, 2005 1:36:20 PM
  • Last Modified: Jul 24, 2014 11:59:34 AM
Revisions
  • Version: 2 public model Download this version
    • Submitted on: Jul 24, 2014 11:59:34 AM
    • Submitted by: Nicolas Le Novère
    • With comment: Current version of Gardner1998 - Cell Cycle Goldbeter
  • Version: 1 public model Download this version
    • Submitted on: Sep 13, 2005 1:36:20 PM
    • Submitted by: Nicolas Le Novère
    • With comment: Original import of BIOMD0000000008.xml.origin
Curator's comment:
(added: 10 Aug 2009, 15:53:31, updated: 10 Aug 2009, 15:53:31)
Figure 4B of the reference publication is reproduced here. The model was simulated using Copasi v4.5 (Build 30)