Li2009- Assymetric Caulobacter cell cycle
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Ashley Xavier
PROVIDER: BIOMD0000000727 | BioModels | 2019-07-12
REPOSITORIES: BioModels
Publications
Temporal controls of the asymmetric cell division cycle in Caulobacter crescentus.
Li Shenghua S Brazhnik Paul P Sobral Bruno B Tyson John J JJ
PLoS computational biology 20090814 8
The asymmetric cell division cycle of Caulobacter crescentus is orchestrated by an elaborate gene-protein regulatory network, centered on three major control proteins, DnaA, GcrA and CtrA. The regulatory network is cast into a quantitative computational model to investigate in a systematic fashion how these three proteins control the relevant genetic, biochemical and physiological properties of proliferating bacteria. Different controls for both swarmer and stalked cell cycles are represented in ...[more]
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Project description:This a model from the article:
A Data-Driven, Mathematical Model of Mammalian Cell Cycle Regulation.
Michael C. Weis, Jayant Avva, James W. Jacobberger, Sree N. Sreenath PLoS ONE
2014 May 13: 9(5): e97130 24824602
,
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.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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.
2018-11-22 | BIOMD0000000723 | BioModels
Project 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.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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.
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This is a hypothetical model of cell cycle that describes the molecular mechanism for regulating DNA synthesis, bud emergence, mitosis, and cell division in budding yeast.
This model is described in the article:
Integrative analysis of cell cycle control in budding yeast.
Chen KC, Calzone L, Csikasz-Nagy A, Cross FR, Novak B, Tyson JJ
Mol. Biol. Cell. [2004 Aug; Volume: 15 (Issue: 8 )] Page info: 3841-62
Abstract:
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The model reproduces the time profiles of the different species in Figure 2 of the paper. The figure depicts the cycle of a daughter cell. Since the Mass Doubling Time (MDT) is 90 minutes, time t=90 from the model simulation will correspond to time t=0 in the paper. The model was successfully tested using MathSBML and SBML odeSolver.
To create a valid SBML file, a local parameter k=1 was added in the reaction 'Inactivation_274_CDC20'. Also, in order to annotate the protein and to have the interaction in the reaction graph to match figure 1 of the article, the reaction rate constants k_{mad2}, k_{bub2} and k_{lte1} are considered as species and renamed as MAD2, BUB2 and LTE1 in the model.
This model is hosted on BioModels Database
and identified by: BIOMD0000000056
.
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.
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