Abstract
Vibrio cholerae, the causative agent of the cholera disease, is commonly used as a model organism for the study of bacteria with multipartite genomes. Its two chromosomes of different sizes initiate their DNA replication at distinct time points in the cell cycle and terminate in synchrony. In this study, the time-delayed start of Chr2 was verified in a synchronized cell population. This replication pattern suggests two possible regulation mechanisms for other Vibrio species with different sized secondary chromosomes: Either all Chr2 start DNA replication with a fixed delay after Chr1 initiation, or the timepoint at which Chr2 initiates varies such that termination of chromosomal replication occurs in synchrony. We investigated these two models and revealed that the two chromosomes of various Vibrionaceae species terminate in synchrony while Chr2-initiation timing relative to Chr1 is variable. Moreover, the sequence and function of the Chr2-triggering crtS site recently discovered in V. cholerae were found to be conserved, explaining the observed timing mechanism. Our results suggest that it is beneficial for bacterial cells with multiple chromosomes to synchronize their replication termination, potentially to optimize chromosome related processes as dimer resolution or segregation.
Highlights
The diversity of regulatory systems of DNA replication has been studied in multiple bacteria [1,2,3,4]
Our results indicate that a synchronous termination of the two chromosomes in this group of bacterial species is under evolutionary selection, suggesting it to be potentially important for the process of cell division
In synchronized V. cholerae cell cultures, such a time delay should lead to a situation with only Chr1 replicating in all cells short after initiation and later Chr2 replication
Summary
The diversity of regulatory systems of DNA replication has been studied in multiple bacteria [1,2,3,4]. In the search for regulatory mechanisms of communication between the two chromosomes, it was found that Chr was insensitive to the blockage of Chr replication [26]: it was shown that Chr controls replication of Chr through a short sequence about 800 kbp downstream from ori1 [27]. This site was later named crtS, for ‘Chr replication triggering site’ [25]. The mechanism underlying the triggering effect of crtS is not yet fully understood but might involve physical contacts that were observed to occur between crtS and ori2 [25]
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