ArticleProceedings of the National Academy of Sciences of the United States of America2014
Completion of DNA replication in Escherichia coli.
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 58 papers.
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Who cites it
58 citing papers in PubMed.
- RecBCD Prevents Bacterial Autoimmunity by Clearing Self-DNA Ends Produced During Replication Termination.bioRxiv : the preprint server for biology · 2026Article
- Topoisomerase III limits RecA-dependent DNA amplification in the chromosome terminus with RecG.Nucleic acids research · 2026Article
- The bacterial MRE11-RAD50 and DNA2-WRN homologs process replication forks at distinct and separate loci on the chromosome.FEBS letters · 2026Article
- Termination of DNA replication drives genomic instability via multiple mechanisms.Nucleic acids research · 2026Article
- Mechanisms of chromosomal DNA replication in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2026Review
- Conflicts between the DNA replication and repair machineries promote cell death in Gram-positive bacteria.Microbiology (Reading, England) · 2025Article
- The RecBC complex protects single-stranded DNA gaps during lesion bypass.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Topo IV is required to allow replisomes to converge and complete replication on the chromosome.PLoS genetics · 2025Article
- In vivo single-molecule imaging of RecB reveals efficient repair of DNA damage in Escherichia coli.Nucleic acids research · 2025Article
- The effect of site-specific recombinases XerCD on the removal of over-replicated chromosomal DNA through outer membrane vesicles in bacteria.Microbiology spectrum · 2024Article
- Advances and applications of CRISPR/Cas-mediated interference inEngineering microbiology · 2024Review
- Genome replication in asynchronously growing microbial populations.PLoS computational biology · 2024Article
- RecBCD enzyme: mechanistic insights from mutants of a complex helicase-nuclease.Microbiology and molecular biology reviews : MMBR · 2023Review
- Gene duplication and deletion caused by over-replication at a fork barrier.Nature communications · 2023Article
- Bacterial Argonaute nucleases reveal different modes of DNA targeting in vitro and in vivo.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
- Host nucleases generate prespacers for primed adaptation in theScience advances · 2022Article
- Role for DNA double strand end-resection activity of RecBCD in control of aberrant chromosomal replication initiation in Escherichia coli.Nucleic acids research · 2022Article
- Speed variations of bacterial replisomes.eLife · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The mechanism by which cells recognize and complete replicated regions at their precise doubling point must be remarkably efficient, occurring thousands of times per cell division along the chromosomes of humans. However, this process remains poorly understood. Here we show that, in Escherichia coli, the completion of replication involves an enzymatic system that effectively counts pairs and limits cellular replication to its doubling point by allowing converging replication forks to transiently continue through the doubling point before the excess, over-replicated regions are incised, resected, and joined. Completion requires RecBCD and involves several proteins associated with repairing double-strand breaks including, ExoI, SbcDC, and RecG. However, unlike double-strand break repair, completion occurs independently of homologous recombination and RecA. In some bacterial viruses, the completion mechanism is specifically targeted for inactivation to allow over-replication to occur during lytic replication. The results suggest that a primary cause of genomic instabilities in many double-strand-break-repair mutants arises from an impaired ability to complete replication, independent from DNA damage.
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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.