Functionality of Two Origins of Replication in Vibrio cholerae Strains With a Single Chromosome

Chromosomal inheritance in bacteria usually entails bidirectional replication of a single chromosome from a single origin into two copies and subsequent partitioning of one copy each into daughter cells upon cell division. However, the human pathogen and other harbor two chromosomes, a large Chr1 an...

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Published in:Frontiers in microbiology Vol. 9; p. 2932
Main Authors: Bruhn, Matthias, Schindler, Daniel, Kemter, Franziska S., Wiley, Michael R., Chase, Kitty, Koroleva, Galina I., Palacios, Gustavo, Sozhamannan, Shanmuga, Waldminghaus, Torsten
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media S.A 30.11.2018
Subjects:
DNA replication
Microbiology
multipartite genome
pathogens
plasmid
replication initiation
secondary chromosome
multipartite genome
DNA replication
pathogens
secondary chromosome
plasmid
cholera
replication initiation
ISSN:1664-302X, 1664-302X
Online Access:Get full text
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Summary:Chromosomal inheritance in bacteria usually entails bidirectional replication of a single chromosome from a single origin into two copies and subsequent partitioning of one copy each into daughter cells upon cell division. However, the human pathogen and other harbor two chromosomes, a large Chr1 and a small Chr2. Chr1 and Chr2 have different origins, an type origin and a P1 plasmid-type origin, respectively, driving the replication of respective chromosomes. Recently, we described naturally occurring exceptions to the two-chromosome rule of : i.e., Chr1 and Chr2 fused single chromosome strains, NSCV1 and NSCV2, in which both origins of replication are present. Using NSCV1 and NSCV2, here we tested whether two types of origins of replication can function simultaneously on the same chromosome or one or the other origin is silenced. We found that in NSCV1, both origins are active whereas in NSCV2 is silenced despite the fact that it is functional in an isolated context. The activity appears to be primarily determined by the copy number of the triggering site, which in turn is determined by its location with respect to and on the fused chromosome.
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Edited by: Alan Leonard, Florida Institute of Technology, United States
Reviewed by: Dhruba Chattoraj, National Institutes of Health (NIH), United States; Ole Skovgaard, Roskilde University, Denmark; Gregory Marczynski, McGill University, Canada
This article was submitted to Evolutionary and Genomic Microbiology, a section of the journal Frontiers in Microbiology
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2018.02932