Li2008 - Caulobacter Cell Cycle

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Short description

This a model from the article:
A Quantitative Study of the Division Cycle of Caulobacter crescentus Stalked Cells.
Shenghua Li, Paul Brazhnik, Bruno Sobral, John J. Tyson PLoS Comput Biol 2008 Jan 25:4(1): e9 18225942 ,
Abstract:
Progression of a cell through the division cycle is tightly controlled at different steps to ensure the integrity of genome replication and partitioning to daughter cells. From published experimental evidence, we propose a molecular mechanism for control of the cell division cycle in Caulobacter crescentus. The mechanism, which is based on the synthesis and degradation of three ‘‘master regulator’’ proteins (CtrA, GcrA, and DnaA), is converted into a quantitative model, in order to study the temporal dynamics of these and other cell cycle proteins. The model accounts for important details of the physiology, biochemistry, and genetics of cell cycle control in stalked C. crescentus cell. It reproduces protein time courses in wild-type cells, mimics correctly the phenotypes of many mutant strains, and predicts the phenotypes of currently uncharacterized mutants. Since many of the proteins involved in regulating the cell cycle of C. crescentus are conserved among many genera of a-proteobacteria, the proposed mechanism may be applicable to other species of importance in agriculture and medicine.

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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

Format
SBML (L2V4)
Related Publication
  • A quantitative study of the division cycle of Caulobacter crescentus stalked cells.
  • Li S, Brazhnik P, Sobral B, Tyson JJ
  • PLoS computational biology , 1/ 2008 , Volume 4 , Issue 1 , pages: e9
  • Department of Biological Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, United States of America.
  • Progression of a cell through the division cycle is tightly controlled at different steps to ensure the integrity of genome replication and partitioning to daughter cells. From published experimental evidence, we propose a molecular mechanism for control of the cell division cycle in Caulobacter crescentus. The mechanism, which is based on the synthesis and degradation of three "master regulator" proteins (CtrA, GcrA, and DnaA), is converted into a quantitative model, in order to study the temporal dynamics of these and other cell cycle proteins. The model accounts for important details of the physiology, biochemistry, and genetics of cell cycle control in stalked C. crescentus cell. It reproduces protein time courses in wild-type cells, mimics correctly the phenotypes of many mutant strains, and predicts the phenotypes of currently uncharacterized mutants. Since many of the proteins involved in regulating the cell cycle of C. crescentus are conserved among many genera of alpha-proteobacteria, the proposed mechanism may be applicable to other species of importance in agriculture and medicine.
Contributors
Ashley Xavier

Metadata information

hasProperty
Gene Ontology regulation of cell cycle
Gene Ontology cell cycle
hasTaxon
Curation status
Curated
Name Description Size Actions

Model file

Li2008.xml SBML lvl2 file containing the model 171.52 KB Preview | Download

Additional files

Li2008_reactions.cps copasi file to generate figure 4 206.61 KB Preview | Download

  • Model originally submitted by : Ashley Xavier
  • Submitted: 07-Nov-2018 13:23:02
  • Last Modified: 07-Nov-2018 13:23:02
Revisions
  • Version: 2 public model Download this version
    • Submitted on: 07-Nov-2018 13:23:02
    • Submitted by: Ashley Xavier
    • With comment: Automatically added model identifier BIOMD0000000718
Curator's comment:
(added: 07 Nov 2018, 13:19:12, updated: 07 Nov 2018, 13:21:39)
Unlike the publication description Zring = 0 is never achieved in the simulations, a reset condition of Zring < 0.11 was used and it reproduced the publication figure 4 accurately. The simulations were done using COPASI 4.24 and plotted in R 3.5.1.