In contrast to proteins recognizing small-molecule ligands, DNA-dependent enzymes cannot rely solely on interactions in the substrate-binding centre to achieve their exquisite specificity. It is widely believed that substrate recognition by such enzymes involves a series of conformational changes in the enzyme-DNA complex with sequential gates favoring cognate DNA and rejecting nonsubstrates. However, direct evidence for such mechanism is limited to a few systems. We report that discrimination between the oxidative DNA lesion, 8-oxoguanine (oxoG) and its normal counterpart, guanine, by the repair enzyme, formamidopyrimidine-DNA glycosylase (Fpg), likely involves multiple gates. Fpg uses an aromatic wedge to open the Watson-Crick base pair and everts the lesion into its active site. We used molecular dynamics simulations to explore the eversion free energy landscapes of oxoG and G by Fpg, focusing on structural and energetic details of oxoG recognition. The resulting energy profiles, supported by biochemical analysis of site-directed mutants disturbing the interactions along the proposed path, show that Fpg selectively facilitates eversion of oxoG by stabilizing several intermediate states, helping the rapidly sliding enzyme avoid full extrusion of every encountered base for interrogation. Lesion recognition through multiple gating intermediates may be a common theme in DNA repair enzymes.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4737139 | PMC |
http://dx.doi.org/10.1093/nar/gkv1092 | DOI Listing |
Talanta
February 2025
State Key Laboratory of Analytical Chemistry for Life Science, School of Chemistry and Chemical Engineering, Nanjing University, Nanjing, 210023, China. Electronic address:
Food Funct
October 2024
Centre for Animal Sciences and Veterinary Studies (CECAV), University of Trás-os-Montes and Alto Douro, 5000-801 Vila Real, Portugal.
The integrity of the genome is under constant threat from both endogenous and exogenous factors that induce oxidative stress and accelerate ageing. The demand for natural and organic cosmetics is rising due to the harmful effects of synthetic genotoxic agents on human health and the environment. Elderberry ( L.
View Article and Find Full Text PDFFree Radic Biol Med
August 2024
Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway; Department of Clinical Service, Division of Cancer Medicine, Oslo University Hospital, Oslo, Norway.
DNA damage caused by oxidative reactions plays a crucial role in the pathogenesis of colorectal cancer (CRC). In a previous cross-sectional study, CRC patients diagnosed with regional disease (stage III) exhibited a higher level of DNA base oxidation in peripheral blood mononuclear cells (PBMCs) 2-9 months post-surgery compared to those with localized disease (stage I-II). To further explore this observation over time, the present study aimed to investigate DNA base oxidation in CRC patients with localized versus regional disease 6 and 12 months after the initial measurements.
View Article and Find Full Text PDFMutat Res Genet Toxicol Environ Mutagen
March 2024
Univ. Grenoble Alpes, CNRS, UMR 5525, VetAgro Sup, Grenoble INP, TIMC, 38000 Grenoble, France. Electronic address:
Preclinical and clinical studies have shown that molecular hydrogen (H) has anti-oxidant, anti-inflammatory, and anti-apoptotic properties. Safety data are available in the literature and acute toxicity has been tested in isolated cells and laboratory animals. We have evaluates the genotoxicity of H in vivo in rats after 72 h exposure, following the International Council for Harmonization guidelines ICH S2 (R1).
View Article and Find Full Text PDFDNA Repair (Amst)
February 2024
Rutgers Center for Lipid Research, Rutgers University, New Brunswick, NJ, USA; Center for Microbiome, Nutrition, and Health, New Jersey Institute for Food, Nutrition, and Health, Rutgers University, New Brunswick, NJ, USA; Department of Nutritional Sciences, Rutgers University, New Brunswick, NJ, USA. Electronic address:
Oxidative stress-induced DNA base modifications, if unrepaired, can increase mutagenesis and genomic instability, ultimately leading to cell death. Cells predominantly use the base excision repair (BER) pathway to repair oxidatively-induced non-helix distorting lesions. BER is initiated by DNA glycosylases, such as 8-oxoguanine DNA glycosylase (OGG1), which repairs oxidatively modified guanine bases, including 7,8-dihydro-8-oxoguanine (8-oxoG) and ring-opened formamidopyrimidine lesions, 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG).
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!