ArticlePLoS genetics2016
RecG Directs DNA Synthesis during Double-Strand Break Repair.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- Topoisomerase III limits RecA-dependent DNA amplification in the chromosome terminus with RecG.Nucleic acids research · 2026Article
- RecBCD-dependent post-UV replication restart inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading.Nature communications · 2025Article
- Antibacterial Effect and Mechanism of Chelerythrine onMicroorganisms · 2025Article
- Isolation and purification of DNA double-strand break repair intermediates for understanding complex molecular mechanisms.PloS one · 2024Article
- Identification ofJournal of bacteriology · 2023Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- Replication fork binding triggers structural changes in the PriA helicase that govern DNA replication restart in E. coli.Nature communications · 2023Article
- Interaction with the carboxy-terminal tip of SSB is critical for RecG function in E. coli.Nucleic acids research · 2023Article
- Characterization of a pathway of genomic instability induced by R-loops and its regulation by topoisomerases in E. coli.PLoS genetics · 2023Article
- Interplay between chromosomal architecture and termination of DNA replication in bacteria.Frontiers in microbiology · 2023Review
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- Essential Role for an Isoform of Escherichia coli Translation Initiation Factor IF2 in Repair of Two-Ended DNA Double-Strand Breaks.Journal of bacteriology · 2022Article
- A commensal-encoded genotoxin drives restriction ofProceedings of the National Academy of Sciences of the United States of America · 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
- Topoisomerase I Essentiality, DnaA-Independent Chromosomal Replication, and Transcription-Replication Conflict in Escherichia coli.Journal of bacteriology · 2021Article
- Distribution of Holliday junctions and repair forks during Escherichia coli DNA double-strand break repair.PLoS genetics · 2021Article
- Article
- Effects of Conserved Wedge Domain Residues on DNA Binding Activity ofFrontiers in genetics · 2021Article
- Stimulation of homologous recombination in plants expressing heterologous recombinases.BMC plant biology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Homologous recombination provides a mechanism of DNA double-strand break repair (DSBR) that requires an intact, homologous template for DNA synthesis. When DNA synthesis associated with DSBR is convergent, the broken DNA strands are replaced and repair is accurate. However, if divergent DNA synthesis is established, over-replication of flanking DNA may occur with deleterious consequences. The RecG protein of Escherichia coli is a helicase and translocase that can re-model 3-way and 4-way DNA structures such as replication forks and Holliday junctions. However, the primary role of RecG in live cells has remained elusive. Here we show that, in the absence of RecG, attempted DSBR is accompanied by divergent DNA replication at the site of an induced chromosomal DNA double-strand break. Furthermore, DNA double-stand ends are generated in a recG mutant at sites known to block replication forks. These double-strand ends, also trigger DSBR and the divergent DNA replication characteristic of this mutant, which can explain over-replication of the terminus region of the chromosome. The loss of DNA associated with unwinding joint molecules previously observed in the absence of RuvAB and RecG, is suppressed by a helicase deficient PriA mutation (priA300), arguing that the action of RecG ensures that PriA is bound correctly on D-loops to direct DNA replication rather than to unwind joint molecules. This has led us to put forward a revised model of homologous recombination in which the re-modelling of branched intermediates by RecG plays a fundamental role in directing DNA synthesis and thus maintaining genomic stability.
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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.