ArticleThe Journal of biological chemistry2019
The recombination mediator proteins RecFOR maintain RecA* levels for maximal DNA polymerase V Mut activity.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Abrogation of SOS mutagenesis by themSystems · 2026Article
- Rescuing the bacterial replisome at a nick requires recombinational repair and helicase reloading.Nature communications · 2025Article
- The Role of the RecFOR Complex in Genome Stability.International journal of molecular sciences · 2025Review
- Ultrasonic cavitation induced Vibrio parahaemolyticus entering an apoptosis-like death process through SOS response.Ultrasonics sonochemistry · 2024Article
- RecF protein targeting to postreplication (daughter strand) gaps I: DNA binding by RecF and RecFR.Nucleic acids research · 2023Article
- Single strand gap repair: The presynaptic phase plays a pivotal role in modulating lesion tolerance pathways.PLoS genetics · 2022Article
- Review
- MicroRNA let-7i Inhibits Histone Lysine Demethylase KDM5B to Halt Esophageal Cancer Progression.Molecular therapy. Nucleic acids · 2020Article
- Two components of DNA replication-dependent LexA cleavage.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA template damage can potentially block DNA replication. Cells have therefore developed different strategies to repair template lesions. Activation of the bacterial lesion bypass DNA polymerase V (Pol V) requires both the cleavage of the UmuD subunit to UmuD' and the acquisition of a monomer of activated RecA recombinase, forming Pol V Mut. Both of these events are mediated by the generation of RecA* via the formation of a RecA-ssDNA filament during the SOS response. Formation of RecA* is itself modulated by competition with the ssDNA-binding protein (SSB) for binding to ssDNA. Previous observations have demonstrated that RecA filament formation on SSB-coated DNA can be favored in the presence of the recombination mediator proteins RecF, RecO, and RecR. We show here using purified proteins that in the presence of SSB and RecA, a stable RecA-ssDNA filament is not formed, although sufficient RecA* is generated to support some activation of Pol V. The presence of RecFOR increased RecA* generation and allowed Pol V to synthesize longer DNA products and to elongate from an unpaired primer terminus opposite template damage, also without the generation of a stable RecA-ssDNA filament.
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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.