ArticleG3 (Bethesda, Md.)2022
Identification of genetic interactions with priB links the PriA/PriB DNA replication restart pathway to double-strand DNA break repair in Escherichia coli.
Article in G3 (Bethesda, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Domain dynamics within the PriA DNA helicase regulate DNA replication restart.Nucleic acids research · 2026Article
- Visualization of the complete preprimosome reveals the structural mechanisms governing DNA replication restart.Nature communications · 2026Article
- A hybrid Ornstein-Uhlenbeck-Branching framework unifies microbial and pediatric tumor evolution.Frontiers in oncology · 2026Article
- Altering translation allows E. coli to overcome G-quadruplex stabilizers.Nucleic acids research · 2025Article
- Proteomic profiling ofTurkish journal of biology = Turk biyoloji dergisi · 2025Article
- The crystal structure of bacteriophage λ RexA provides novel insights into the DNA binding properties of Rex-like phage exclusion proteins.Nucleic acids research · 2024Article
- Identification ofJournal of bacteriology · 2023Article
- Replication fork binding triggers structural changes in the PriA helicase that govern DNA replication restart in E. coli.Nature communications · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Collisions between DNA replication complexes (replisomes) and impediments such as damaged DNA or proteins tightly bound to the chromosome lead to premature dissociation of replisomes at least once per cell cycle in Escherichia coli. Left unrepaired, these events produce incompletely replicated chromosomes that cannot be properly partitioned into daughter cells. DNA replication restart, the process that reloads replisomes at prematurely terminated sites, is therefore essential in E. coli and other bacteria. Three replication restart pathways have been identified in E. coli: PriA/PriB, PriA/PriC, and PriC/Rep. A limited number of genetic interactions between replication restart and other genome maintenance pathways have been defined, but a systematic study placing replication restart reactions in a broader cellular context has not been performed. We have utilized transposon-insertion sequencing to identify new genetic interactions between DNA replication restart pathways and other cellular systems. Known genetic interactors with the priB replication restart gene (uniquely involved in the PriA/PriB pathway) were confirmed and several novel priB interactions were discovered. Targeted genetic and imaging-based experiments with priB and its genetic partners revealed significant double-strand DNA break accumulation in strains with mutations in dam, rep, rdgC, lexA, or polA. Modulating the activity of the RecA recombinase partially suppressed the detrimental effects of rdgC or lexA mutations in ΔpriB cells. Taken together, our results highlight roles for several genes in double-strand DNA break homeostasis and define a genetic network that facilitates DNA repair/processing upstream of PriA/PriB-mediated DNA replication restart in E. coli.
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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.