ArticleNucleic acids research2012
Replication regulation of Vibrio cholerae chromosome II involves initiator binding to the origin both as monomer and as dimer.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Dynamic transitions of initiator binding coordinate the replication of the two chromosomes in Vibrio cholerae.Nature communications · 2025Article
- The replication enhancer crtS depends on transcription factor Lrp for modulating binding of initiator RctB to ori2 of Vibrio cholerae.Nucleic acids research · 2024Article
- Cell cycle-coordinated maintenance of theEcoSal Plus · 2023Review
- Rep protein accommodates together dsDNA and ssDNA which enables a loop-back mechanism to plasmid DNA replication initiation.Nucleic acids research · 2023Article
- The dimerization interface of initiator RctB governs chaperone and enhancer dependence of Vibrio cholerae chromosome 2 replication.Nucleic acids research · 2022Article
- The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator.Nucleic acids research · 2021Article
- Interactions of replication initiator RctB with single- and double-stranded DNA in origin opening of Vibrio cholerae chromosome 2.Nucleic acids research · 2020Article
- Vibrio cholerae chromosome 2 copy number is controlled by the methylation-independent binding of its monomeric initiator to the chromosome 1 crtS site.Nucleic acids research · 2018Article
- Chromosome 1 licenses chromosome 2 replication in Vibrio cholerae by doubling the crtS gene dosage.PLoS genetics · 2018Article
- Synchronous termination of replication of the two chromosomes is an evolutionary selected feature in Vibrionaceae.PLoS genetics · 2018Article
- Replicate Once Per Cell Cycle: Replication Control of Secondary Chromosomes.Frontiers in microbiology · 2018Review
- Establishing a System for Testing Replication Inhibition of the Vibrio cholerae Secondary Chromosome in Escherichia coli.Antibiotics (Basel, Switzerland) · 2017Article
- The replication initiator of the cholera pathogen's second chromosome shows structural similarity to plasmid initiators.Nucleic acids research · 2017Article
- Article
- Random versus Cell Cycle-Regulated Replication Initiation in Bacteria: Insights from Studying Vibrio cholerae Chromosome 2.Microbiology and molecular biology reviews : MMBR · 2017Review
- A checkpoint control orchestrates the replication of the two chromosomes of Vibrio cholerae.Science advances · 2016Article
- Optimization and Characterization of the Synthetic Secondary Chromosome synVicII inFrontiers in bioengineering and biotechnology · 2016Article
- Article
- Chromosome I controls chromosome II replication in Vibrio cholerae.PLoS genetics · 2014Article
- Initiator protein dimerization plays a key role in replication control of Vibrio cholerae chromosome 2.Nucleic acids research · 2014Article
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4 authors.
Funding
Abstract
The origin region of Vibrio cholerae chromosome II (chrII) resembles plasmid origins that have repeated initiator-binding sites (iterons). Iterons are essential for initiation as well as preventing over-initiation of plasmid replication. In chrII, iterons are also essential for initiation but over-initiation is prevented by sites called 39-mers. Both iterons and 39-mers are binding sites of the chrII specific initiator, RctB. Here, we have isolated RctB mutants that permit over-initiation in the presence of 39-mers. Characterization of two of the mutants showed that both are defective in 39-mer binding, which helps to explain their over-initiation phenotype. In vitro, RctB bound to 39-mers as monomers, and to iterons as both monomers and dimers. Monomer binding to iterons increased in both the mutants, suggesting that monomers are likely to be the initiators. We suggest that dimers might be competitive inhibitors of monomer binding to iterons and thus help control replication negatively. ChrII replication was found to be dependent on chaperones DnaJ and DnaK in vivo. The chaperones preferentially improved dimer binding in vitro, further suggesting the importance of dimer binding in the control of chrII replication.
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