Scholarlink

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

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

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

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年1月8日

查看全文
  • 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,
  • Marie-Eve Val

摘要

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.