ArticlePLoS genetics2022
Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways.
Article in PLoS genetics, 2022. 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, 10 citations in OpenAlex.
- Visualizing the interplay of Cas1-Cas2 with DNA replication-repair that creates CRISPR-Cas immunity.Nucleic acids research · 2026Article
- Spatiotemporal characterization of single-stranded DNA Intermediates after UV Irradiation: I: Post-replication gaps formed during slow growth.PLoS genetics · 2026Article
- Spatiotemporal characterization of single-stranded DNA intermediates after UV irradiation: II. Rapid growth and effects of recA and recJ.PLoS genetics · 2026Article
- 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
- Post-replicative lesion processing limits DNA damage-induced mutagenesis.Nucleic acids research · 2025Article
- Hallmarks of DNA replication stress responses in Escherichia coli and Bacillus subtilis.FEMS microbiology reviews · 2025Review
- A bipartite interaction with the processivity clamp potentiates Pol IV-mediated TLS.bioRxiv : the preprint server for biology · 2024Article
- Generation and Repair of Postreplication Gaps in Escherichia coli.Microbiology and molecular biology reviews : MMBR · 2023Review
- RecF protein targeting to postreplication (daughter strand) gaps I: DNA binding by RecF and RecFR.Nucleic acids research · 2023Article
- RecF protein targeting to post-replication (daughter strand) gaps II: RecF interaction with replisomes.Nucleic acids research · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During replication, the presence of unrepaired lesions results in the formation of single stranded DNA (ssDNA) gaps that need to be repaired to preserve genome integrity and cell survival. All organisms have evolved two major lesion tolerance pathways to continue replication: Translesion Synthesis (TLS), potentially mutagenic, and Homology Directed Gap Repair (HDGR), that relies on homologous recombination. In Escherichia coli, the RecF pathway repairs such ssDNA gaps by processing them to produce a recombinogenic RecA nucleofilament during the presynaptic phase. In this study, we show that the presynaptic phase is crucial for modulating lesion tolerance pathways since the competition between TLS and HDGR occurs at this stage. Impairing either the extension of the ssDNA gap (mediated by the nuclease RecJ and the helicase RecQ) or the loading of RecA (mediated by RecFOR) leads to a decrease in HDGR and a concomitant increase in TLS. Hence, we conclude that defects in the presynaptic phase delay the formation of the D-loop and increase the time window allowed for TLS. In contrast, we show that a defect in the postsynaptic phase that impairs HDGR does not lead to an increase in TLS. Unexpectedly, we also reveal a strong genetic interaction between recF and recJ genes, that results in a recA deficient-like phenotype in which HDGR is almost completely abolished.
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