Dataset Information


Novak1997 - Cell Cycle

ABSTRACT: Novak1997 - Cell Cycle Modeling the control of DNA replication in fission yeast. This model is described in the article: Modeling the control of DNA replication in fission yeast. Novak B., Tyson JJ. Proc. Natl. Acad. Sci. U.S.A. 1997:94(17):9147-52 Abstract: A central event in the eukaryotic cell cycle is the decision to commence DNA replication (S phase). Strict controls normally operate to prevent repeated rounds of DNA replication without intervening mitoses ("endoreplication") or initiation of mitosis before DNA is fully replicated ("mitotic catastrophe"). Some of the genetic interactions involved in these controls have recently been identified in yeast. From this evidence we propose a molecular mechanism of "Start" control in Schizosaccharomyces pombe. Using established principles of biochemical kinetics, we compare the properties of this model in detail with the observed behavior of various mutant strains of fission yeast: wee1(-) (size control at Start), cdc13Delta and rum1(OP) (endoreplication), and wee1(-) rum1Delta (rapid division cycles of diminishing cell size). We discuss essential features of the mechanism that are responsible for characteristic properties of Start control in fission yeast, to expose our proposal to crucial experimental tests. This model is hosted on BioModels Database and identified by: BIOMD0000000007 . To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models . To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Nicolas Le Novère  

PROVIDER: BIOMD0000000007 | BioModels | 2009-10-15


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Finishing the cell cycle.

Novák B   Tóth A   Csikász-Nagy A   Györffy B   Tyson JJ   Nasmyth K  

Journal of theoretical biology 19990701 2

The eukaryotic cell division cycle consists of two characteristic states: G1, when replication origins of chromosomes are in a pre-replicative state, and S/G2/M, when they are in a post-replicative state (Nasmyth, 1995). Using straightforward biochemical kinetics, we show that these two states can be created by antagonistic interactions between cyclin-dependent kinases (Cdk) and their foes: the cyclin-degradation machinery (APC) and a stoichiometric inhibitor (CKI). Irreversible transitions betw  ...[more]

Publication: 1/2

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