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Recognition of DNA Lesions

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 July 2020) | Viewed by 60397

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Special Issue Editors

Dr. Joanna Timmins

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Guest Editor

Univ. Grenoble Alpes, CNRS, CEA, IBS, F-38000 Grenoble, France
Interests: DNA damage and repair; integrated structural biology; Deinococcus radiodurans; nucleoid organization and dynamics; radiation resistance; cancer and anticancer drug resistance

Dr. Jean-Luc Ravanat

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Co-Guest Editor

Univ. Grenoble Alpes, CEA, CNRS, IRIG/DIESE/SyMMES, F-38000 Grenoble, France
Interests: DNA damage and repair; chemistry and biochemistry of DNA & RNA; radiation biology; photobiology; oxidative stress; detection of cellular DNA damage; epigenetic DNA modifications; radiosensitization

Special Issue Information

Dear Colleagues,

The average human cell develops over 10,000 DNA lesions per day. If left unrepaired, the damaged DNA results in replication errors, mutations, and genomic instability, that ultimately threaten cell and organism viability. Cells have evolved elaborate mechanisms to detect and repair DNA lesions, and the wide diversity of DNA lesions necessitates multiple, largely distinct DNA repair mechanisms. In all cases, DNA repair typically occurs in four steps: (i) damage detection, (ii) damage verification, (iii) damage removal, and (iv) resynthesis of DNA. The first step, DNA damage recognition, is a very challenging cellular process involving the detection of rare modifications to the DNA within a large pool of intact genomic material. The specificity and efficiency of molecular recognition is achieved by the formation of dynamic macromolecular complexes at sites of DNA damage and the regulated handoff of DNA repair intermediates to the subsequent repair enzyme. In this Special Issue, the focus will be on the molecular mechanisms devised by prokaryotic and eukaryotic cells to efficiently recognize and remove a wide range of chemically and structurally diverse DNA lesions from genomic DNA during the early steps of DNA damage response.

Dr. Joanna Timmins
Dr. Jean-Luc Ravanat
Guest Editors

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Keywords

DNA lesions
DNA lesion recognition
DNA repair
dynamics
molecular interactions
conformational plasticity
genomic instability
mutations
substrate specificity

Published Papers (14 papers)

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Editorial

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4 pages, 203 KiB

Open AccessEditorial

Recognition of DNA Lesions

by Joanna Timmins

Int. J. Mol. Sci. 2023, 24(11), 9682; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24119682 - 02 Jun 2023

Viewed by 777

Abstract

The average human cell suffers from approximately 10⁴–10⁵ DNA lesions per day [...] Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

Research

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12 pages, 1503 KiB

Open AccessArticle

C-Terminal Extensions of Ku70 and Ku80 Differentially Influence DNA End Binding Properties

by Takabumi Inagawa, Thomas Wennink, Joyce H. G. Lebbink, Guido Keijzers, Bogdan I. Florea, Nicole S. Verkaik and Dik C. van Gent

Int. J. Mol. Sci. 2020, 21(18), 6725; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186725 - 14 Sep 2020

Cited by 8 | Viewed by 2582

Abstract

The Ku70/80 heterodimer binds to DNA ends and attracts other proteins involved in the non-homologous end-joining (NHEJ) pathway of DNA double-strand break repair. We developed a novel assay to measure DNA binding and release kinetics using differences in Förster resonance energy transfer (FRET) of the ECFP-Ku70/EYFP-Ku80 heterodimer in soluble and DNA end bound states. We confirmed that the relative binding efficiencies of various DNA substrates (blunt, 3 nucleotide 5′ extension, and DNA hairpin) measured in the FRET assay reflected affinities obtained from direct measurements using surface plasmon resonance. The FRET assay was subsequently used to investigate Ku70/80 behavior in the context of a DNA-dependent kinase (DNA-PK) holocomplex. As expected, this complex was much more stable than Ku70/80 alone, and its stability was influenced by DNA-PK phosphorylation status. Interestingly, the Ku80 C-terminal extension contributed to DNA-PK complex stability but was not absolutely required for its formation. The Ku70 C-terminal SAP domain, on the other hand, was required for the stable association of Ku70/80 to DNA ends, but this effect was abrogated in DNA-PK holocomplexes. We conclude that FRET measurements can be used to determine Ku70/80 binding kinetics. The ability to do this in complex mixtures makes this assay particularly useful to study larger NHEJ protein complexes on DNA ends. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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19 pages, 7697 KiB

Open AccessArticle

Comparison of High- and Low-LET Radiation-Induced DNA Double-Strand Break Processing in Living Cells

by Stefan J. Roobol, Irene van den Bent, Wiggert A. van Cappellen, Tsion E. Abraham, Maarten W. Paul, Roland Kanaar, Adriaan B. Houtsmuller, Dik C. van Gent and Jeroen Essers

Int. J. Mol. Sci. 2020, 21(18), 6602; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186602 - 09 Sep 2020

Cited by 39 | Viewed by 4778

Abstract

High-linear-energy-transfer (LET) radiation is more lethal than similar doses of low-LET radiation types, probably a result of the condensed energy deposition pattern of high-LET radiation. Here, we compare high-LET α-particle to low-LET X-ray irradiation and monitor double-strand break (DSB) processing. Live-cell microscopy was used to monitor DNA double-strand breaks (DSBs), marked by p53-binding protein 1 (53BP1). In addition, the accumulation of the endogenous 53BP1 and replication protein A (RPA) DSB processing proteins was analyzed by immunofluorescence. In contrast to α-particle-induced 53BP1 foci, X-ray-induced foci were resolved quickly and more dynamically as they showed an increase in 53BP1 protein accumulation and size. In addition, the number of individual 53BP1 and RPA foci was higher after X-ray irradiation, while focus intensity was higher after α-particle irradiation. Interestingly, 53BP1 foci induced by α-particles contained multiple RPA foci, suggesting multiple individual resection events, which was not observed after X-ray irradiation. We conclude that high-LET α-particles cause closely interspaced DSBs leading to high local concentrations of repair proteins. Our results point toward a change in DNA damage processing toward DNA end-resection and homologous recombination, possibly due to the depletion of soluble protein in the nucleoplasm. The combination of closely interspaced DSBs and perturbed DNA damage processing could be an explanation for the increased relative biological effectiveness (RBE) of high-LET α-particles compared to X-ray irradiation. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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15 pages, 3463 KiB

Open AccessArticle

USP14 Regulates DNA Damage Response and Is a Target for Radiosensitization in Non-Small Cell Lung Cancer

by Arishya Sharma and Alexandru Almasan

Int. J. Mol. Sci. 2020, 21(17), 6383; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176383 - 02 Sep 2020

Cited by 20 | Viewed by 2794

Abstract

Non-small cell lung cancer (NSCLC) represents ~85% of the lung cancer cases. Despite recent advances in NSCLC treatment, the five-year survival rate is still around 23%. Radiotherapy is indicated in the treatment of both early and advanced stage NSCLC; however, treatment response in patients is heterogeneous. Thus, identification of new and more effective treatment combinations is warranted. We have identified Ubiquitin-specific protease 14 (USP14) s a regulator of major double-strand break (DSB) repair pathways in response to ionizing radiation (IR) by its impact on both non-homologous end joining (NHEJ) and homologous recombination (HR) in NSCLC. USP14 is a proteasomal deubiquitinase. IR treatment increases levels and DSB recruitment of USP14 in NSCLC cell lines. Genetic knockdown, using shUSP14 expression or pharmacological inhibition of USP14, using IU1, increases radiosensitization in NSCLC cell lines, as determined by a clonogenic survival assay. Moreover, shUSP14-expressing NSCLC cells show increased NHEJ efficiency, as indicated by chromatin recruitment of key NHEJ proteins, NHEJ reporter assay, and increased IR-induced foci formation by 53BP1 and pS2056-DNA-PKcs. Conversely, shUSP14-expressing NSCLC cells show decreased RPA32 and BRCA1 foci formation, suggesting HR-deficiency. These findings identify USP14 as an important determinant of DSB repair in response to radiotherapy and a promising target for NSCLC radiosensitization. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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9 pages, 1372 KiB

Open AccessArticle

Involvement of POLA2 in Double Strand Break Repair and Genotoxic Stress

by Tuyen T. Dang and Julio C. Morales

Int. J. Mol. Sci. 2020, 21(12), 4245; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124245 - 15 Jun 2020

Cited by 9 | Viewed by 2667

Abstract

Cellular survival is dependent on the efficient replication and transmission of genomic information. DNA damage can be introduced into the genome by several different methods, one being the act of DNA replication. Replication is a potent source of DNA damage and genomic instability, especially through the formation of DNA double strand breaks (DSBs). DNA polymerase alpha is responsible for replication initiation. One subunit of the DNA polymerase alpha replication machinery is POLA2. Given the connection between replication and genomic instability, we decided to examine the role of POLA2 in DSB repair, as little is known about this topic. We found that loss of POLA2 leads to an increase in spontaneous DSB formation. Loss of POLA2 also slows DSB repair kinetics after treatment with etoposide and inhibits both of the major double strand break repair pathways: non-homologous end-joining and homologous recombination. In addition, loss of POLA2 leads to increased sensitivity to ionizing radiation and PARP1 inhibition. Lastly, POLA2 expression is elevated in glioblastoma multiforme tumors and correlates with poor overall patient survival. These data demonstrate a role for POLA2 in DSB repair and resistance to genotoxic stress. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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18 pages, 2201 KiB

Open AccessArticle

DNA Damage Regulates Senescence-Associated Extracellular Vesicle Release via the Ceramide Pathway to Prevent Excessive Inflammatory Responses

by Kazuhiro Hitomi, Ryo Okada, Tze Mun Loo, Kenichi Miyata, Asako J. Nakamura and Akiko Takahashi

Int. J. Mol. Sci. 2020, 21(10), 3720; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21103720 - 25 May 2020

Cited by 47 | Viewed by 5915

Abstract

DNA damage, caused by various oncogenic stresses, can induce cell death or cellular senescence as an important tumor suppressor mechanism. Senescent cells display the features of a senescence-associated secretory phenotype (SASP), secreting inflammatory proteins into surrounding tissues, and contributing to various age-related pathologies. In addition to this inflammatory protein secretion, the release of extracellular vesicles (EVs) is also upregulated in senescent cells. However, the molecular mechanism underlying this phenomenon remains unclear. Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis. The EV biogenesis pathway, together with the autophagy-mediated degradation pathway, functions to block apoptosis by removing cytoplasmic DNA fragments derived from chromosomal DNA or bacterial infections. Our data suggest that this SA-EV pathway may play a prominent role in cellular homeostasis, particularly in senescent cells. In summary, DNA damage provokes SA-EV release by activating the ceramide pathway to protect cells from excessive inflammatory responses. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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14 pages, 2800 KiB

Open AccessArticle

Norepinephrine-Induced DNA Damage in Ovarian Cancer Cells

by Rocio Lamboy-Caraballo, Carmen Ortiz-Sanchez, Arelis Acevedo-Santiago, Jaime Matta, Alvaro N.A. Monteiro and Guillermo N. Armaiz-Pena

Int. J. Mol. Sci. 2020, 21(6), 2250; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21062250 - 24 Mar 2020

Cited by 23 | Viewed by 4611

Abstract

Multiple studies have shown that psychological distress in epithelial ovarian cancer (EOC) patients is associated with worse quality of life and poor treatment adherence. This may influence chemotherapy response and prognosis. Moreover, although stress hormones can reduce cisplatin efficacy in EOC treatment, their effect on the integrity of DNA remains poorly understood. In this study, we investigated whether norepinephrine and epinephrine can induce DNA damage and modulate cisplatin-induced DNA damage in three EOC cell lines. Our data show that norepinephrine and epinephrine exposure led to increased nuclear γ-H2AX foci formation in EOC cells, a marker of double-strand DNA breaks. We further characterized norepinephrine-induced DNA damage by subjecting EOC cells to alkaline and neutral comet assays. Norepinephrine exposure caused DNA double-strand breaks, but not single-strand breaks. Interestingly, pre-treatment with propranolol abrogated norepinephrine-induced DNA damage indicating that its effects may be mediated by β-adrenergic receptors. Lastly, we determined the effects of norepinephrine on cisplatin-induced DNA damage. Our data suggest that norepinephrine reduced cisplatin-induced DNA damage in EOC cells and that this effect may be mediated independently of β-adrenergic receptors. Taken together, these results suggest that stress hormones can affect DNA integrity and modulate cisplatin resistance in EOC cells. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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Review

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23 pages, 35611 KiB

Open AccessReview

The Multifaceted Roles of Ku70/80

by Sayma Zahid, Murielle Seif El Dahan, Florence Iehl, Paloma Fernandez-Varela, Marie-Helene Le Du, Virginie Ropars and Jean Baptiste Charbonnier

Int. J. Mol. Sci. 2021, 22(8), 4134; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084134 - 16 Apr 2021

Cited by 42 | Viewed by 6374

Abstract

DNA double-strand breaks (DSBs) are accidental lesions generated by various endogenous or exogenous stresses. DSBs are also genetically programmed events during the V(D)J recombination process, meiosis, or other genome rearrangements, and they are intentionally generated to kill cancer during chemo- and radiotherapy. Most DSBs are processed in mammalian cells by the classical nonhomologous end-joining (c-NHEJ) pathway. Understanding the molecular basis of c-NHEJ has major outcomes in several fields, including radiobiology, cancer therapy, immune disease, and genome editing. The heterodimer Ku70/80 (Ku) is a central actor of the c-NHEJ as it rapidly recognizes broken DNA ends in the cell and protects them from nuclease activity. It subsequently recruits many c-NHEJ effectors, including nucleases, polymerases, and the DNA ligase 4 complex. Beyond its DNA repair function, Ku is also involved in several other DNA metabolism processes. Here, we review the structural and functional data on the DNA and RNA recognition properties of Ku implicated in DNA repair and in telomeres maintenance. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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25 pages, 2002 KiB

Open AccessReview

Role of Oxidative DNA Damage and Repair in Atrial Fibrillation and Ischemic Heart Disease

by Liangyu Hu, Zhengkun Wang, Claudia Carmone, Jaap Keijer and Deli Zhang

Int. J. Mol. Sci. 2021, 22(8), 3838; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083838 - 07 Apr 2021

Cited by 24 | Viewed by 4084

Abstract

Atrial fibrillation (AF) and ischemic heart disease (IHD) represent the two most common clinical cardiac diseases, characterized by angina, arrhythmia, myocardial damage, and cardiac dysfunction, significantly contributing to cardiovascular morbidity and mortality and posing a heavy socio-economic burden on society worldwide. Current treatments of these two diseases are mainly symptomatic and lack efficacy. There is thus an urgent need to develop novel therapies based on the underlying pathophysiological mechanisms. Emerging evidence indicates that oxidative DNA damage might be a major underlying mechanism that promotes a variety of cardiac diseases, including AF and IHD. Antioxidants, nicotinamide adenine dinucleotide (NAD⁺) boosters, and enzymes involved in oxidative DNA repair processes have been shown to attenuate oxidative damage to DNA, making them potential therapeutic targets for AF and IHD. In this review, we first summarize the main molecular mechanisms responsible for oxidative DNA damage and repair both in nuclei and mitochondria, then describe the effects of oxidative DNA damage on the development of AF and IHD, and finally discuss potential targets for oxidative DNA repair-based therapeutic approaches for these two cardiac diseases. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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20 pages, 22622 KiB

Open AccessReview

A Peek Inside the Machines of Bacterial Nucleotide Excision Repair

by Thanyalak Kraithong, Silas Hartley, David Jeruzalmi and Danaya Pakotiprapha

Int. J. Mol. Sci. 2021, 22(2), 952; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020952 - 19 Jan 2021

Cited by 18 | Viewed by 6573

Abstract

Double stranded DNA (dsDNA), the repository of genetic information in bacteria, archaea and eukaryotes, exhibits a surprising instability in the intracellular environment; this fragility is exacerbated by exogenous agents, such as ultraviolet radiation. To protect themselves against the severe consequences of DNA damage, cells have evolved at least six distinct DNA repair pathways. Here, we review recent key findings of studies aimed at understanding one of these pathways: bacterial nucleotide excision repair (NER). This pathway operates in two modes: a global genome repair (GGR) pathway and a pathway that closely interfaces with transcription by RNA polymerase called transcription-coupled repair (TCR). Below, we discuss the architecture of key proteins in bacterial NER and recent biochemical, structural and single-molecule studies that shed light on the lesion recognition steps of both the GGR and the TCR sub-pathways. Although a great deal has been learned about both of these sub-pathways, several important questions, including damage discrimination, roles of ATP and the orchestration of protein binding and conformation switching, remain to be addressed. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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26 pages, 2178 KiB

Open AccessReview

Focus on DNA Glycosylases—A Set of Tightly Regulated Enzymes with a High Potential as Anticancer Drug Targets

by Fabienne Hans, Muge Senarisoy, Chandini Bhaskar Naidu and Joanna Timmins

Int. J. Mol. Sci. 2020, 21(23), 9226; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21239226 - 03 Dec 2020

Cited by 6 | Viewed by 3622

Abstract

Cancer is the second leading cause of death with tens of millions of people diagnosed with cancer every year around the world. Most radio- and chemotherapies aim to eliminate cancer cells, notably by causing severe damage to the DNA. However, efficient repair of such damage represents a common mechanism of resistance to initially effective cytotoxic agents. Thus, development of new generation anticancer drugs that target DNA repair pathways, and more particularly the base excision repair (BER) pathway that is responsible for removal of damaged bases, is of growing interest. The BER pathway is initiated by a set of enzymes known as DNA glycosylases. Unlike several downstream BER enzymes, DNA glycosylases have so far received little attention and the development of specific inhibitors of these enzymes has been lagging. Yet, dysregulation of DNA glycosylases is also known to play a central role in numerous cancers and at different stages of the disease, and thus inhibiting DNA glycosylases is now considered a valid strategy to eliminate cancer cells. This review provides a detailed overview of the activities of DNA glycosylases in normal and cancer cells, their modes of regulation, and their potential as anticancer drug targets. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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18 pages, 1292 KiB

Open AccessReview

Lost in the Crowd: How Does Human 8-Oxoguanine DNA Glycosylase 1 (OGG1) Find 8-Oxoguanine in the Genome?

by Ostiane D’Augustin, Sébastien Huet, Anna Campalans and Juan Pablo Radicella

Int. J. Mol. Sci. 2020, 21(21), 8360; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21218360 - 07 Nov 2020

Cited by 17 | Viewed by 5947

Abstract

The most frequent DNA lesion resulting from an oxidative stress is 7,8-dihydro-8-oxoguanine (8-oxoG). 8-oxoG is a premutagenic base modification due to its capacity to pair with adenine. Thus, the repair of 8-oxoG is critical for the preservation of the genetic information. Nowadays, 8-oxoG is also considered as an oxidative stress-sensor with a putative role in transcription regulation. In mammalian cells, the modified base is excised by the 8-oxoguanine DNA glycosylase (OGG1), initiating the base excision repair (BER) pathway. OGG1 confronts the massive challenge that is finding rare occurrences of 8-oxoG among a million-fold excess of normal guanines. Here, we review the current knowledge on the search and discrimination mechanisms employed by OGG1 to find its substrate in the genome. While there is considerable data from in vitro experiments, much less is known on how OGG1 is recruited to chromatin and scans the genome within the cellular nucleus. Based on what is known of the strategies used by proteins searching for rare genomic targets, we discuss the possible scenarios allowing the efficient detection of 8-oxoG by OGG1. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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11 pages, 1157 KiB

Open AccessReview

Using a Human Papillomavirus Model to Study DNA Replication and Repair of Wild Type and Damaged DNA Templates in Mammalian Cells

by Dipon Das, Molly L. Bristol, Pietro Pichierri and Iain M. Morgan

Int. J. Mol. Sci. 2020, 21(20), 7564; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21207564 - 13 Oct 2020

Cited by 2 | Viewed by 2832

Abstract

Human papillomaviruses have 8kbp DNA episomal genomes that replicate autonomously from host DNA. During initial infection, the virus increases its copy number to 20–50 copies per cell, causing torsional stress on the replicating DNA. This activates the DNA damage response (DDR) and HPV replicates its genome, at least in part, using homologous recombination. An active DDR is on throughout the HPV life cycle. Two viral proteins are required for replication of the viral genome; E2 binds to 12bp palindromic sequences around the A/T rich origin of replication and recruits the viral helicase E1 via a protein–protein interaction. E1 forms a di-hexameric complex that replicates the viral genome in association with host factors. Transient replication assays following transfection with E1–E2 expression plasmids, along with an origin containing plasmid, allow monitoring of E1-E2 replication activity. Incorporating a bacterial lacZ gene into the origin plasmid allows for the determination of replication fidelity. Here we describe how we exploited this system to investigate replication and repair in mammalian cells, including using damaged DNA templates. We propose that this system has the potential to enhance the understanding of cellular components involved in DNA replication and repair. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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23 pages, 3157 KiB

Open AccessReview

Formation and Recognition of UV-Induced DNA Damage within Genome Complexity

by Philippe Johann to Berens and Jean Molinier

Int. J. Mol. Sci. 2020, 21(18), 6689; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186689 - 12 Sep 2020

Cited by 26 | Viewed by 6188

Abstract

Ultraviolet (UV) light is a natural genotoxic agent leading to the formation of photolesions endangering the genomic integrity and thereby the survival of living organisms. To prevent the mutagenetic effect of UV, several specific DNA repair mechanisms are mobilized to accurately maintain genome integrity at photodamaged sites within the complexity of genome structures. However, a fundamental gap remains to be filled in the identification and characterization of factors at the nexus of UV-induced DNA damage, DNA repair, and epigenetics. This review brings together the impact of the epigenomic context on the susceptibility of genomic regions to form photodamage and focuses on the mechanisms of photolesions recognition through the different DNA repair pathways. Full article

(This article belongs to the Special Issue Recognition of DNA Lesions)

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