ArticleJournal of bacteriology2002
Nitric oxide-induced homologous recombination in Escherichia coli is promoted by DNA glycosylases.
Article in Journal of bacteriology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- Co-evolution of gene transfer agents and their alphaproteobacterial hosts.Journal of bacteriology · 2024Article
- The SMC-like RecN protein is at the crossroads of several genotoxic stress responses inFrontiers in microbiology · 2023Article
- Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol-induced neuronal nitric oxide synthase uncoupling in metastatic osteosarcoma cells.Redox biology · 2020Article
- The bacterial DNA repair protein Mfd confers resistance to the host nitrogen immune response.Scientific reports · 2016Article
- Article
- A unique uracil-DNA binding protein of the uracil DNA glycosylase superfamily.Nucleic acids research · 2015Article
- XRCC1 and base excision repair balance in response to nitric oxide.DNA repair · 2011Article
- Detrimental effects of hypoxia-specific expression of uracil DNA glycosylase (Ung) in Mycobacterium smegmatis.Journal of bacteriology · 2010Article
- Single cell trapping and DNA damage analysis using microwell arrays.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Analysis of the impact of a uracil DNA glycosylase attenuated in AP-DNA binding in maintenance of the genomic integrity in Escherichia coli.Nucleic acids research · 2010Article
- The Base Excision Repair system of Salmonella enterica serovar typhimurium counteracts DNA damage by host nitric oxide.PLoS pathogens · 2009Article
- Arylphosphonium salts interact with DNA to modulate cytotoxicity.Mutation research · 2009Article
- Article
- Antimutator role of the DNA glycosylase mutY gene in Helicobacter pylori.Journal of bacteriology · 2006Article
- RecA and RadA proteins of Brucella abortus do not perform overlapping protective DNA repair functions following oxidative burst.Journal of bacteriology · 2006Article
- A genome-wide distribution of 8-oxoguanine correlates with the preferred regions for recombination and single nucleotide polymorphism in the human genome.Genome research · 2006Article
- Threshold effects of nitric oxide-induced toxicity and cellular responses in wild-type and p53-null human lymphoblastoid cells.Chemical research in toxicology · 2006Article
- Inhibition of bacterial DNA replication by zinc mobilization during nitrosative stress.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Repair system for noncanonical purines in Escherichia coli.Journal of bacteriology · 2003Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO*) is involved in neurotransmission, inflammation, and many other biological processes. Exposure of cells to NO* leads to DNA damage, including formation of deaminated and oxidized bases. Apurinic/apyrimidinic (AP) endonuclease-deficient cells are sensitive to NO* toxicity, which indicates that base excision repair (BER) intermediates are being generated. Here, we show that AP endonuclease-deficient cells can be protected from NO* toxicity by inactivation of the uracil (Ung) or formamidopyrimidine (Fpg) DNA glycosylases but not by inactivation of a 3-methyladenine (AlkA) DNA glycosylase. These results suggest that Ung and Fpg remove nontoxic NO*-induced base damage to create BER intermediates that are toxic if they are not processed by AP endonucleases. Our next goal was to learn how Ung and Fpg affect susceptibility to homologous recombination. The RecBCD complex is critical for repair of double-strand breaks via homologous recombination. When both Ung and Fpg were inactivated in recBCD cells, survival was significantly enhanced. We infer that both Ung and Fpg create substrates for recombinational repair, which is consistent with the observation that disrupting ung and fpg suppressed NO*-induced recombination. Taken together, a picture emerges in which the action of DNA glycosylases on NO*-induced base damage results in the accumulation of BER intermediates, which in turn can induce homologous recombination. These studies shed light on the underlying mechanism of NO*-induced homologous recombination.
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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.