ArticleGenetics2010
Promoting and avoiding recombination: contrasting activities of the Escherichia coli RuvABC Holliday junction resolvase and RecG DNA translocase.
Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- SspA is a transcriptional regulator of CRISPR adaptation in E. coli.Nucleic acids research · 2025Article
- Identification ofJournal of bacteriology · 2023Article
- Robust linear DNA degradation supports replication-initiation-defective mutants in Escherichia coli.G3 (Bethesda, Md.) · 2022Article
- ArsR Family Regulator MSMEG_6762 Mediates the Programmed Cell Death by Regulating the Expression of HNH Nuclease in Mycobacteria.Microorganisms · 2022Article
- Modulation of RecFORQ- and RecA-Mediated Homologous Recombination in Escherichia coli by Isoforms of Translation Initiation Factor IF2.Journal of bacteriology · 2022Article
- The rarA gene as part of an expanded RecFOR recombination pathway: Negative epistasis and synthetic lethality with ruvB, recG, and recQ.PLoS genetics · 2021Article
- Too Much of a Good Thing: How Ectopic DNA Replication Affects Bacterial Replication Dynamics.Frontiers in microbiology · 2020Review
- Chromosomal over-replication in Escherichia coli recG cells is triggered by replication fork fusion and amplified if replichore symmetry is disturbed.Nucleic acids research · 2018Article
- Xer Site Specific Recombination: Double and Single Recombinase Systems.Frontiers in microbiology · 2017Review
- 25 years on and no end in sight: a perspective on the role of RecG protein.Current genetics · 2016Article
- Different genome stability proteins underpin primed and naïve adaptation in E. coli CRISPR-Cas immunity.Nucleic acids research · 2015Article
- The RECG1 DNA Translocase Is a Key Factor in Recombination Surveillance, Repair, and Segregation of the Mitochondrial DNA in Arabidopsis.The Plant cell · 2015Article
- Regression of replication forks stalled by leading-strand template damage: I. Both RecG and RuvAB catalyze regression, but RuvC cleaves the holliday junctions formed by RecG preferentially.The Journal of biological chemistry · 2014Article
- Branch migration prevents DNA loss during double-strand break repair.PLoS genetics · 2014Article
- Cellular location and activity of Escherichia coli RecG proteins shed light on the function of its structurally unresolved C-terminus.Nucleic acids research · 2014Article
- Modulation of DNA damage tolerance in Escherichia coli recG and ruv strains by mutations affecting PriB, the ribosome and RNA polymerase.Molecular microbiology · 2012Article
- Superfamily 2 helicases.Frontiers in bioscience (Landmark edition) · 2012Review
- On the viability of Escherichia coli cells lacking DNA topoisomerase I.BMC microbiology · 2012Article
- Article
- The C-terminal domain of the bacterial SSB protein acts as a DNA maintenance hub at active chromosome replication forks.PLoS genetics · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
RuvABC and RecG are thought to provide alternative pathways for the late stages of recombination in Escherichia coli. Inactivation of both blocks the recovery of recombinants in genetic crosses. RuvABC resolves Holliday junctions, with RuvAB driving branch migration and RuvC catalyzing junction cleavage. RecG also drives branch migration, but no nuclease has been identified that might act with RecG to cleave junctions, apart from RusA, which is not normally expressed. We searched for an alternative nuclease using a synthetic lethality assay to screen for mutations causing inviability in the absence of RuvC, on the premise that a strain without any ability to cut junctions might be inviable. All the mutations identified mapped to polA, dam, or uvrD. None of these genes encodes a nuclease that cleaves Holliday junctions. Probing the reason for the inviability using the RusA Holliday junction resolvase provided strong evidence in each case that the RecG pathway is very ineffective at removing junctions and indicated that a nuclease component most probably does not exist. It also revealed new suppressors of recG, which were located to the ssb gene. Taken together with the results from the synthetic lethality assays, the properties of the mutant SSB proteins provide evidence that, rather than promoting recombination, a major function of RecG is to curb potentially pathological replication initiated via PriA protein at sites remote from oriC.
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Registered trials
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.