Format

Send to

Choose Destination
PLoS Genet. 2018 Mar 5;14(3):e1007251. doi: 10.1371/journal.pgen.1007251. eCollection 2018 Mar.

Synchronous termination of replication of the two chromosomes is an evolutionary selected feature in Vibrionaceae.

Author information

1
LOEWE Center for Synthetic Microbiology-SYNMIKRO, Philipps-Universität Marburg, Marburg, Germany.
2
Leibniz Institute DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig, Germany.
3
Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, Santa Cruz, United States of America.
4
German Centre of Infection Research (DZIF), Partner Site Hannover-Braunschweig, Braunschweig, Germany.

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.

PMID:
29505558
PMCID:
PMC5854411
DOI:
10.1371/journal.pgen.1007251
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center