ArticleJournal of bacteriology2009
CtrA, a global response regulator, uses a distinct second category of weak DNA binding sites for cell cycle transcription control in Caulobacter crescentus.
Article in Journal of bacteriology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- LD-transpeptidation is crucial for fitness and polar growth in Agrobacterium tumefaciens.PLoS genetics · 2024Article
- Computational modeling of unphosphorylated CtrA:iScience · 2021Article
- Nucleoid-associated proteins shape chromatin structure and transcriptional regulation across the bacterial kingdom.Transcription · 2021Review
- Selective sequestration of signalling proteins in a membraneless organelle reinforces the spatial regulation of asymmetry in Caulobacter crescentus.Nature microbiology · 2020Article
- Absolute Measurements of mRNA Translation in Caulobacter crescentus Reveal Important Fitness Costs of Vitamin BmSystems · 2019Article
- Periplasmic protein EipA determines envelope stress resistance and virulence in Brucella abortus.Molecular microbiology · 2019Article
- Architecture of divergent flagellar promoters controlled by CtrA in Rhodobacter sphaeroides.BMC microbiology · 2018Article
- Sensory domain of the cell cycle kinase CckA regulates the differential DNA binding of the master regulator CtrA in Caulobacter crescentus.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
- Use of a Phosphorylation Site Mutant To Identify Distinct Modes of Gene Repression by the Control of Virulence Regulator (CovR) in Streptococcus pyogenes.Journal of bacteriology · 2017Article
- VAP, a Versatile Access Point for the Endoplasmic Reticulum: Review and analysis of FFAT-like motifs in the VAPome.Biochimica et biophysica acta · 2016Review
- Dynamical Localization of DivL and PleC in the Asymmetric Division Cycle of Caulobacter crescentus: A Theoretical Investigation of Alternative Models.PLoS computational biology · 2015Article
- The global regulatory architecture of transcription during the Caulobacter cell cycle.PLoS genetics · 2015Article
- Redefining bacterial origins of replication as centralized information processors.Frontiers in microbiology · 2015Review
- Expanding the direct HetR regulon in Anabaena sp. strain PCC 7120.Journal of bacteriology · 2014Article
- Effect of a ctrA promoter mutation, causing a reduction in CtrA abundance, on the cell cycle and development of Caulobacter crescentus.BMC microbiology · 2013Article
- Global mapping of transcription start sites and promoter motifs in the symbiotic α-proteobacterium Sinorhizobium meliloti 1021.BMC genomics · 2013Article
- Transcriptional regulation of the Rhodobacter capsulatus response regulator CtrA.Microbiology (Reading, England) · 2013Article
- The Caulobacter crescentus ctrA P1 promoter is essential for the coordination of cell cycle events that prevent the overinitiation of DNA replication.Microbiology (Reading, England) · 2012Article
- Article
- Insights into the CtrA regulon in development of stress resistance in obligatory intracellular pathogen Ehrlichia chaffeensis.Molecular microbiology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CtrA controls cell cycle programs of chromosome replication and genetic transcription. Phosphorylated CtrA approximately P exhibits high affinity (dissociation constant [K(d)], <10 nM) for consensus TTAA-N7-TTAA binding sites with "typical" (N = 7) spacing. We show here that ctrA promoters P1 and P2 use low-affinity (K(d), >500 nM) CtrA binding sites with "atypical" (N not equal 7) spacing. Footprints demonstrated that phosphorylated CtrA approximately P does not exhibit increased affinity for "atypical" sites, as it does for sites in the replication origin. Instead, high levels of CtrA (>10 microM) accumulate, which can drive CtrA binding to "atypical" sites. In vivo cross-linking showed that when the stable CtrADelta3 protein persists during the cell cycle, the "atypical" sites at ctrA and motB are persistently bound. Interestingly, the cell cycle timing of ctrA P1 and P2 transcription is not altered by persistent CtrADelta3 binding. Therefore, operator DNA occupancy is not sufficient for regulation, and it is the cell cycle variation of CtrA approximately P phosphorylation that provides the dominant "activation" signal. Protein dimerization is one potential means of "activation." The glutathione S-transferase (GST) protein dimerizes, and fusion with CtrA (GST-CtrA) creates a stable dimer with enhanced affinity for TTAA motifs. Electrophoretic mobility shift assays with GST-CtrA revealed cooperative modes of binding that further distinguish the "atypical" sites. GST-CtrA also binds a single TTAA motif in ctrA P1 aided by DNA in the extended TTAACCAT motif. We discuss how "atypical" sites are a common yet distinct category of CtrA regulatory sites and new implications for the working and evolution of cell cycle control networks.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.