Dynamic transitions of initiator binding coordinate the replication of the two chromosomes in Vibrio cholerae

Théophile Niault, Ariel Talavera, Eric Le Cam, Sonia Baconnais, Ole Skovgaard, Florian Fournes, Léa Wagner, Hedvig Tamman, Andrew Thompson, Dannele Echemendia-Blanco, Noa Guzzi, Abel Garcia-Pino (), Didier Mazel () and Marie-Eve Val ()
Additional contact information
Théophile Niault: Département Génomes et Génétique
Ariel Talavera: Boulevard du Triomphe
Eric Le Cam: Gustave Roussy
Sonia Baconnais: Gustave Roussy
Ole Skovgaard: Roskilde University
Florian Fournes: Département Génomes et Génétique
Léa Wagner: Département Génomes et Génétique
Hedvig Tamman: Boulevard du Triomphe
Andrew Thompson: Saint-Aubin - BP48
Dannele Echemendia-Blanco: Boulevard du Triomphe
Noa Guzzi: Département Génomes et Génétique
Abel Garcia-Pino: Boulevard du Triomphe
Didier Mazel: Département Génomes et Génétique
Marie-Eve Val: Département Génomes et Génétique

Nature Communications, 2025, vol. 16, issue 1, 1-16

Abstract: Abstract The replication of the two chromosomes in the pathogenic bacterium Vibrio cholerae is coordinated by the binding of initiator protein RctB to a checkpoint sequence, crtS. Replication of crtS on the primary chromosome (Chr1) triggers replication of the secondary chromosome (Chr2), but the details are poorly understood. Here, we analyze RctB binding patterns in the V. cholerae genome across various cell cycle stages. We find that RctB primarily binds to sites inhibiting replication initiation at the Chr2 origin (ori2). This inhibitory effect is counteracted when crtS is replicated on Chr1, causing a shift in RctB binding to sites that activate replication at ori2. Structural analyzes indicate the formation of diverse oligomeric states of RctB, coupled to the allosteric effect of DNA, which determine ori2 accessibility. We propose a synchronization model where, upon replication, crtS locally destabilizes the RctB inhibition complex, releasing the Chr2 replication origin.

Date: 2025
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DOI: 10.1038/s41467-024-55598-9

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