ArticleBiochimica et biophysica acta. Gene regulatory mechanisms2018
Sensory domain of the cell cycle kinase CckA regulates the differential DNA binding of the master regulator CtrA in Caulobacter crescentus.
Article in Biochimica et biophysica acta. Gene regulatory mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Nucleotide composition shapes gene expression inmSystems · 2025Article
- TheJournal of bacteriology · 2024Article
- Tuning Microbial Activity via Programmatic Alteration of Cell/Substrate Interfaces.Advanced materials (Deerfield Beach, Fla.) · 2021Review
- Sensing, Signaling, and Secretion: A Review and Analysis of Systems for Regulating Host Interaction inGenes · 2020Review
- Synthesis of histidine kinase inhibitors and their biological properties.Medicinal research reviews · 2020Review
- Selective sequestration of signalling proteins in a membraneless organelle reinforces the spatial regulation of asymmetry in Caulobacter crescentus.Nature microbiology · 2020Article
- Construction of a RobustFrontiers in bioengineering and biotechnology · 2020Article
- Integrated Transcriptional Regulatory Network of Quorum Sensing, Replication Control, and SOS Response inFrontiers in microbiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sophisticated signaling mechanisms allow bacterial cells to cope with environmental and intracellular challenges. Activation of specific pathways ameliorates these challenges and thereby warrants integrity. Here, we demonstrate the pliability of the CckA-CtrA two-component signaling system in the freshwater bacterium Caulobacter crescentus. Our forward genetic screen to analyze suppressor mutations that can negate the chromosome segregation block induced by the topoisomerase IV inhibitor, NstA, yielded various point mutations in the cell cycle histidine kinase, CckA. Notably, we identified a point mutation in the PAS-B domain of CckA, which resulted in increased levels of phosphorylated CtrA (CtrA~P), the master cell cycle regulator. Surprisingly, this increase in CtrA~P levels did not translate into a genome-wide increase in the DNA occupancy of CtrA, but specifically enriched its affinity for the chromosomal origin of replication, C
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Registered trials
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