TY - JOUR
T1 - Dynamic transitions of initiator binding coordinate the replication of the two chromosomes in Vibrio cholerae
AU - Niault, Théophile
AU - Talavera, Ariel
AU - Le Cam, Eric
AU - Baconnais, Sonia
AU - Skovgaard, Ole
AU - Fournes, Florian
AU - Wagner, Léa
AU - Tamman, Hedvig
AU - Thompson, Andrew
AU - Echemendia-Blanco, Dannele
AU - Guzzi, Noa
AU - Garcia-Pino, Abel
AU - Mazel, Didier
AU - Val, Marie Eve
N1 - Publisher Copyright:
© 2025. The Author(s).
PY - 2025/1/8
Y1 - 2025/1/8
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85215073106&partnerID=8YFLogxK
U2 - 10.1038/s41467-024-55598-9
DO - 10.1038/s41467-024-55598-9
M3 - Article
C2 - 39779702
AN - SCOPUS:85215073106
SN - 2041-1723
VL - 16
SP - 485
JO - Nature Communications
JF - Nature Communications
IS - 1
ER -