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Fournes F, Niault T, Czarnecki J, et al. The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator. Nucleic Acids Res. 2021;49(19):11119-11133doi: 10.1093/nar/gkab903.
Fournes, F., Niault, T., Czarnecki, J., Tissier-Visconti, A., Mazel, D., & Val, M. E. (2021). The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator. Nucleic acids research, 49(19), 11119-11133. https://doi.org/10.1093/nar/gkab903
Fournes, Florian, et al. "The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator." Nucleic acids research vol. 49,19 (2021): 11119-11133. doi: https://doi.org/10.1093/nar/gkab903
Fournes F, Niault T, Czarnecki J, Tissier-Visconti A, Mazel D, Val ME. The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator. Nucleic Acids Res. 2021 Nov 08;49(19):11119-11133. doi: 10.1093/nar/gkab903. PMID: 34643717; PMCID: PMC8565311.
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Nucleic Acids Res. 2021 Nov 08;49(19):11119-11133. doi: 10.1093/nar/gkab903.

The coordinated replication of Vibrio cholerae's two chromosomes required the acquisition of a unique domain by the RctB initiator.

Nucleic acids research

Florian Fournes, Theophile Niault, Jakub Czarnecki, Alvise Tissier-Visconti, Didier Mazel, Marie-Eve Val

Affiliations

  1. Institut Pasteur, Université de Paris, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris 75015, France.
  2. Centre National de la Recherche Scientifique, UMR3525, Paris 75015, France.
  3. Sorbonne Université, Collège Doctoral, Paris 75005, France.
  4. University of Warsaw, Department of Bacterial Genetics, Institute of Microbiology, Faculty of Biology, Warsaw 02-096, Poland.

PMID: 34643717 PMCID: PMC8565311 DOI: 10.1093/nar/gkab903

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.

© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.

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