ArticlePLoS computational biology2013
Potential role of a bistable histidine kinase switch in the asymmetric division cycle of Caulobacter crescentus.
Article in PLoS computational biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Turing-pattern model of scaffolding proteins that establish spatial asymmetry during the cell cycle ofiScience · 2023Article
- Computational modeling of unphosphorylated CtrA:iScience · 2021Article
- The interplay of spatial organization and biochemistry in building blocks of cellular signalling pathways.Journal of the Royal Society, Interface · 2020Article
- Reciprocal control of motility and biofilm formation by the PdhS2 two-component sensor kinase of Agrobacterium tumefaciens.Microbiology (Reading, England) · 2019Article
- Noise control for molecular computing.Journal of the Royal Society, Interface · 2018Article
- Stochastic modeling and simulation of reaction-diffusion system with Hill function dynamics.BMC systems biology · 2017Article
- A cell cycle kinase with tandem sensory PAS domains integrates cell fate cues.Nature communications · 2016Article
- Dynamical Localization of DivL and PleC in the Asymmetric Division Cycle of Caulobacter crescentus: A Theoretical Investigation of Alternative Models.PLoS computational biology · 2015Article
- Identification of essential alphaproteobacterial genes reveals operational variability in conserved developmental and cell cycle systems.Molecular microbiology · 2014Article
- Dynamical modeling of the cell cycle and cell fate emergence in Caulobacter crescentus.PloS one · 2014Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The free-living aquatic bacterium, Caulobacter crescentus, exhibits two different morphologies during its life cycle. The morphological change from swarmer cell to stalked cell is a result of changes of function of two bi-functional histidine kinases, PleC and CckA. Here, we describe a detailed molecular mechanism by which the function of PleC changes between phosphatase and kinase state. By mathematical modeling of our proposed molecular interactions, we derive conditions under which PleC, CckA and its response regulators exhibit bistable behavior, thus providing a scenario for robust switching between swarmer and stalked states. Our simulations are in reasonable agreement with in vitro and in vivo experimental observations of wild type and mutant phenotypes. According to our model, the kinase form of PleC is essential for the swarmer-to-stalked transition and to prevent premature development of the swarmer pole. Based on our results, we reconcile some published experimental observations and suggest novel mutants to test our predictions.
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