ArticleNucleic acids research2021
The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator.
Article in Nucleic acids research, 2021. 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, 16 citations in OpenAlex.
- Evidence supporting the first secondary chromosome in Actinobacteria as a hallmark of theMicrobial genomics · 2026Article
- Unraveling the Prevalence and Multifaceted Roles of Accessory Peptide Deformylases in Bacterial Adaptation and Resistance.Molecular biology and evolution · 2025Article
- Genetic determinants of pOXA-48 plasmid maintenance and propagation in Escherichia coli.Nature communications · 2025Article
- 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
- Independent origins and evolution of the secondary replicons of the class Gammaproteobacteria.Microbial genomics · 2023Article
- Recollections of a Helmstetter Disciple.Life (Basel, Switzerland) · 2023Review
- Convergent evolution in two bacterial replicative helicase loaders.Trends in biochemical sciences · 2022Review
- The dimerization interface of initiator RctB governs chaperone and enhancer dependence of Vibrio cholerae chromosome 2 replication.Nucleic acids research · 2022Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Vibrio cholerae, the pathogenic bacterium that causes cholera, has two chromosomes (Chr1, Chr2) that replicate in a well-orchestrated sequence. Chr2 initiation is triggered only after the replication of the crtS site on Chr1. The initiator of Chr2 replication, RctB, displays activities corresponding with its different binding sites: initiator at the iteron sites, repressor at the 39m sites, and trigger at the crtS site. The mechanism by which RctB relays the signal to initiate Chr2 replication from crtS is not well-understood. In this study, we provide new insights into how Chr2 replication initiation is regulated by crtS via RctB. We show that crtS (on Chr1) acts as an anti-inhibitory site by preventing 39m sites (on Chr2) from repressing initiation. The competition between these two sites for RctB binding is explained by the fact that RctB interacts with crtS and 39m via the same DNA-binding surface. We further show that the extreme C-terminal tail of RctB, essential for RctB self-interaction, is crucial for the control exerted by crtS. This subregion of RctB is conserved in all Vibrio, but absent in other Rep-like initiators. Hence, the coordinated replication of both chromosomes likely results from the acquisition of this unique domain by RctB.
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