ArticleProceedings of the National Academy of Sciences of the United States of America2014
XerD-mediated FtsK-independent integration of TLCϕ into the Vibrio cholerae genome.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 27 citations in OpenAlex.
- Prophage border curation reveals horizontal transfer of lysogeny-related elements between filamentous and double jelly-roll phages.Communications biology · 2025Article
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- The Xer activation factor of TLCΦ expands the possibilities for Xer recombination.Nucleic acids research · 2022Article
- Guardian of the Genome: An Alternative RAG/Transib Co-Evolution Hypothesis for the Origin of V(D)J Recombination.Frontiers in immunology · 2021Article
- Evaluation and Differential Diagnosis of a Genetic Marked Brucella Vaccine A19ΔvirB12 for Cattle.Frontiers in immunology · 2021Article
- Identification of novel tetracycline resistance geneEmerging microbes & infections · 2020Article
- Bacillus-infecting bacteriophage Izhevsk harbors thermostable endolysin with broad range specificity.PloS one · 2020Article
- Insights into TLCΦ lysogeny: A twist in the mechanism of IMEX integration.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The TLCΦ satellite phage harbors a Xer recombination activation factor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Mutation Landscape of Base Substitutions, Duplications, and Deletions in the Representative Current Cholera Pandemic Strain.Genome biology and evolution · 2018Article
- Fast growth conditions uncouple the final stages of chromosome segregation and cell division in Escherichia coli.PLoS genetics · 2017Article
- Xer Site Specific Recombination: Double and Single Recombinase Systems.Frontiers in microbiology · 2017Review
- How Xer-exploiting mobile elements overcome cellular control.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- FtsK translocation permits discrimination between an endogenous and an imported Xer/dif recombination complex.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Effect of LexA on Chromosomal Integration of CTXϕ in Vibrio cholerae.Journal of bacteriology · 2016Article
- CTXφ Replication Depends on the Histone-Like HU Protein and the UvrD Helicase.PLoS genetics · 2015Article
- Mechanistic insights into filamentous phage integration in Vibrio cholerae.Frontiers in microbiology · 2014Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As in most bacteria, topological problems arising from the circularity of the two Vibrio cholerae chromosomes, chrI and chrII, are resolved by the addition of a crossover at a specific site of each chromosome, dif, by two tyrosine recombinases, XerC and XerD. The reaction is under the control of a cell division protein, FtsK, which activates the formation of a Holliday Junction (HJ) intermediate by XerD catalysis that is resolved into product by XerC catalysis. Many plasmids and phages exploit Xer recombination for dimer resolution and for integration, respectively. In all cases so far described, they rely on an alternative recombination pathway in which XerC catalyzes the formation of a HJ independently of FtsK. This is notably the case for CTXϕ, the cholera toxin phage. Here, we show that in contrast, integration of TLCϕ, a toxin-linked cryptic satellite phage that is almost always found integrated at the chrI dif site before CTXϕ, depends on the formation of a HJ by XerD catalysis, which is then resolved by XerC catalysis. The reaction nevertheless escapes the normal cellular control exerted by FtsK on XerD. In addition, we show that the same reaction promotes the excision of TLCϕ, along with any CTXϕ copy present between dif and its left attachment site, providing a plausible mechanism for how chrI CTXϕ copies can be eliminated, as occurred in the second wave of the current cholera pandemic.
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