ArticleThe EMBO journal2012
Holliday junction affinity of the base excision repair factor Endo III contributes to cholera toxin phage integration.
Article in The EMBO journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- First Characterization ofViruses · 2024Article
- The TLCΦ satellite phage harbors a Xer recombination activation factor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- 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
- DNA Processing Proteins Involved in the UV-Induced Stress Response of Sulfolobales.Journal of bacteriology · 2015Article
- CTXφ Replication Depends on the Histone-Like HU Protein and the UvrD Helicase.PLoS genetics · 2015Article
- XerD-mediated FtsK-independent integration of TLCϕ into the Vibrio cholerae genome.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- YpfΦ: a filamentous phage acquired by Yersinia pestis.Frontiers in microbiology · 2014Review
- Mechanistic insights into filamentous phage integration in Vibrio cholerae.Frontiers in microbiology · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toxigenic conversion of Vibrio cholerae bacteria results from the integration of a filamentous phage, CTX phage. Integration is driven by the bacterial Xer recombinases, which catalyse the exchange of a single pair of strands between the phage single-stranded DNA and the host double-stranded DNA genomes; replication is thought to convert the resulting pseudo-Holliday junction (HJ) intermediate into the final recombination product. The natural tendency of the Xer recombinases to recycle HJ intermediates back into substrate should thwart this integration strategy, which prompted a search for additional co-factors aiding directionality of the process. Here, we show that Endo III, a ubiquitous base excision repair enzyme, facilitates CTX phage-integration in vivo. In vitro, we show that it prevents futile Xer recombination cycles by impeding new rounds of strand exchanges once the pseudo-HJ is formed. We further demonstrate that this activity relies on the unexpected ability of Endo III to bind to HJs even in the absence of the recombinases. These results explain how tandem copies of the phage genome can be created, which is crucial for subsequent virion production.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.