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Cellular DNA is constantly exposed to endogenous or exogenous factors that can induce lesions. Several types of lesions have been described that can result from UV/ionizing irradiations, oxidative stress, or free radicals, among others. In order to overcome the deleterious effects of such damages, i.e., mutagenicity or cytotoxicity, cells possess a highly complex DNA repair machinery, involving repair enzymes targeting specific types of lesions through dedicated cellular pathways. In addition, DNA is highly compacted in the nucleus, the first level of compaction consisting of ~ 147 DNA base pairs wrapped around a core of histones, the so-called nucleosome core particle. In this complex environment, the DNA structure is highly constrained, and fine-tuned mechanisms involving remodeling processes are required to expose the DNA to repair enzymes and to facilitate the damage removal. However, these nucleosome-specific mechanisms remain poorly understood, and computational methods emerged only recently as powerful tools to investigate DNA damages in such complex systems as the nucleosome. In this mini-review, we summarize the latest advances brought out by computational approaches in the field, opening new exciting perspectives for the study of DNA damage and repair in the nucleosome context., Competing Interests: Competing interestsThe authors declare no competing interests., (© International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)

Objective: The endoscopic findings associated with Helicobacter pylori -naïve status, current infection or past infection are an area of ongoing interest. Previous studies have investigated parameters with a potential diagnostic value. The aim of this study was to perform meta-analysis of the available literature to validate the diagnostic accuracy of mucosal features proposed in the Kyoto classification., Data Sources: The databases of MEDLINE and Embase, clinicalTrials.gov and the Cochrane Library were systematically searched for relevant studies from October 1999 to October 2019., Methods: A bivariate random effects model was used to produce pooled diagnostic accuracy calculations for each of the studied endoscopic findings. Diagnostic odds ratios and sensitivity and specificity characteristics were calculated to identify significant predictors of H pylori status., Results: Meta-analysis included 4380 patients in 15 studies. The most significant predictor of an H pylori -naïve status was a regular arrangement of collecting venules (diagnostic odds ratio 55.0, sensitivity 78.3%, specificity 93.8%). Predictors of active H pylori infection were mucosal oedema (18.1, 63.7%, 91.1%) and diffuse redness (14.4, 66.5%, 89.0%). Map-like redness had high specificity for previous H pylori eradication (99.0%), but poor specificity (13.0%)., Conclusion: The regular arrangement of collecting venules, mucosal oedema, diffuse redness and map-like redness are important endoscopic findings for determining H pylori status. This meta-analysis provides a tentative basis for developing future endoscopic classification systems., Competing Interests: Conflict of interest statement: The authors declared no potential conflicts of interest with respect to the research, authorship and/or publication of this article., (© The Author(s), 2020.)

Eukaryotic transcription-coupled nucleotide excision repair (TC-NER) is a pathway that removes DNA lesions capable of blocking RNA polymerase II (Pol II) transcription from the template strand. This process is initiated by lesion-arrested Pol II and the recruitment of Cockayne Syndrome B protein (CSB). In this review, we will focus on the lesion recognition steps of eukaryotic TC-NER and summarize the recent research progress toward understanding the structural basis of Pol II-mediated lesion recognition and Pol II-CSB interactions. We will discuss the roles of CSB in both TC-NER initiation and transcription elongation. Finally, we propose an updated model of tripartite lesion recognition and verification for TC-NER in which CSB ensures Pol II-mediated recognition of DNA lesions for TC-NER., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The Xeroderma pigmentosum complementation group C protein (XPC) serves as the primary initiating factor in the global genome nucleotide excision repair pathway (GG-NER). Recent reports suggest XPC also stimulates repair of oxidative lesions by base excision repair. However, whether XPC distinguishes among various types of DNA lesions remains unclear. Although the DNA binding properties of XPC have been studied by several groups, there is a lack of consensus over whether XPC discriminates between DNA damaged by lesions associated with NER activity versus those that are not. In this study we report a high-throughput fluorescence anisotropy assay used to measure the DNA binding affinity of XPC for a panel of DNA substrates containing a range of chemical lesions in a common sequence. Our results demonstrate that while XPC displays a preference for binding damaged DNA, the identity of the lesion has little effect on the binding affinity of XPC. Moreover, XPC was equally capable of binding to DNA substrates containing lesions not repaired by GG-NER. Our results suggest XPC may act as a general sensor of damaged DNA that is capable of recognizing DNA containing lesions not repaired by NER., (Copyright © 2013 Elsevier B.V. All rights reserved.)