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Fuse or die: how to survive the loss of Dam in V ibrio cholerae
Author(s) -
Val MarieEve,
Kennedy Sean P.,
SolerBistué Alfonso J.,
Barbe Valérie,
Bouchier Christiane,
DucosGaland Magaly,
Skovgaard Ole,
Mazel Didier
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12483
Subject(s) - biology , vibrio cholerae , homologous recombination , genetics , bacterial artificial chromosome , origin of replication , mutant , dna replication , genome , microbiology and biotechnology , gene , bacteria
Summary Dam methylates GATC sequences in γ‐proteobacteria genomes, regulating several cellular functions including replication. In V ibrio cholerae , which has two chromosomes, Dam is essential for viability, owing to its role in chr2 replication initiation. In this study, we isolated spontaneous mutants of V . cholerae that were able to survive the deletion of dam . In these mutants, homologous recombination and chromosome dimer resolution are essential, unless DNA mismatch repair is inactivated. Furthermore, the initiator of chr2 replication, RctB , is no longer required. We show that, instead, replication of chr2 is insured by spontaneous fusion with chr1 and piggybacking its replication machinery. We report that natural fusion of chr1 and chr2 occurred by two distinct recombination pathways: homologous recombination between repeated IS elements and site‐specific recombination between dif sites. Lastly, we observed a preferential fusion of the two chromosomes in their terminus of replication.