Replication control of multiple chromosomes in bacteria

Transregio TRR 174 Seminar

  • Postponed to 16:15 h
  • Date: Jun 17, 2019
  • Time: 16:15
  • Speaker: Dr. Marie-Eve Kennedy-Val
  • Institut Pasteur, France
  • Location: MPI for Terrestrial Microbiology
  • Room: Lecture hall
  • Host: TRR 174
  • Contact: thanbichler@uni-marburg.de

The canonical model of bacterial genomes posits one essential replicon, the chromosome which harbors all essential housekeeping genes. However, 10% of bacteria have a multipartite genome organization with at least one additional large replicon which may be essential for viability. These large secondary replicons share features of both chromosomes and plasmids, attesting to their plasmid origin. The maintenance of multiple replicons requires complex interplays between chromosomes-specific, plasmid-specific and shared factors to ensure the coordinated replication and segregation of each replicon within the cell cycle. So far, we know very little about the cellular processes that coordinate the maintenance of multiple chromosomes.

Most of our knowledge comes from studies in Vibrio cholerae, which harbors two circular chromosomes, a main chromosome Chr1 (3Mb) and a secondary chromosome Chr2 (1Mb). Both Chr1 and Chr2 carry essential housekeeping genes. Chr1 and Chr2 use distinct initiators for the replication. Chr2 replication origin is closely related to iteron-type plasmids. Despite its plasmid-like vestiges, Chr2 replication timing is chromosome-like, being tightly controlled and occurring only once per cell cycle. Interestingly, Chr1 and Chr2 are replicated in a well-orchestrated manner in such a way that their replication terminates at the same time. Chr2 replication initiation is triggered by the replication of an intergenic sequence (crtS) located on Chr1. This checkpoint mechanism is an elegant and cost-effective way for secondary chromosomes to harmonize their replication with the well-established replication regulatory system of the main chromosome. This mechanism of replication synchronization of Chr1 and Chr2 will be the subject of my presentation.

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