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An insight into understanding the coupling between homologous recombination mediated DNA repair and chromatin remodeling mechanisms in plant genome: an update.
Banerjee, S, Roy, S
Cell cycle (Georgetown, Tex.). 2021;(18):1760-1784
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Abstract
Plants, with their obligatory immobility, are vastly exposed to a wide range of environmental agents and also various endogenous processes, which frequently cause damage to DNA and impose genotoxic stress. These factors subsequently increase genome instability, thus affecting plant growth and productivity. Therefore, to survive under frequent and extreme environmental stress conditions, plants have developed highly efficient and powerful defense mechanisms to repair the damages in the genome for maintaining genome stability. Such multi-dimensional signaling response, activated in presence of damage in the DNA, is collectively known as DNA Damage Response (DDR). DDR plays a crucial role in the remarkably efficient detection, signaling, and repair of damages in the genome for maintaining plant genome stability and normal growth responses. Like other highly advanced eukaryotic systems, chromatin dynamics play a key role in regulating cell cycle progression in plants through remarkable orchestration of environmental and developmental signals. The regulation of chromatin architecture and nucleosomal organization in DDR is mainly modulated by the ATP dependent chromatin remodelers (ACRs), chromatin modifiers, and histone chaperones. ACRs are mainly responsible for transcriptional regulation of several homologous recombination (HR) repair genes in plants under genotoxic stress. The HR-based repair of DNA damage has been considered as the most error-free mechanism of repair and represents one of the essential sources of genetic diversity and new allelic combinations in plants. The initiation of DDR signaling and DNA damage repair pathway requires recruitment of epigenetic modifiers for remodeling of the damaged chromatin while accumulating evidence has shown that chromatin remodeling and DDR share part of the similar signaling pathway through the altered epigenetic status of the associated chromatin region. In this review, we have integrated information to provide an overview on the association between chromatin remodeling mediated regulation of chromatin structure stability and DDR signaling in plants, with emphasis on the scope of the utilization of the available knowledge for the improvement of plant health and productivity.Abbreviation: ADH: Alcohol Dehydrogenase; AGO2: Argonaute 2; ARP: Actin-Related Protein; ASF:1- Anti-Silencing Function-1; ATM: Ataxia Telangiectasia Mutated; ATR: ATM and Rad3- Related; AtSWI3c: Arabidopsis thaliana Switch 3c; ATXR5: Arabidopsis Trithorax-Related5; ATXR6: Arabidopsis Trithorax-Related6; BER: Base Excision Repair; BRCA1: Breast Cancer Associated 1; BRM: BRAHMA; BRU1: BRUSHY1; CAF:1- Chromatin Assembly Factor-1; CHD: Chromodomain Helicase DNA; CHR5: Chromatin Remodeling Protein 5; CHR11/17: Chromatin Remodeling Protein 11/17; CIPK11- CBL- Interacting Protein Kinase 11; CLF: Curly Leaf; CMT3: Chromomethylase 3; COR15A: Cold Regulated 15A; COR47: Cold Regulated 47; CRISPR Clustered Regulatory Interspaced Short Palindromic Repeats; DDM1: Decreased DNA Methylation1; DRR: DNA Repair and Recombination; DSBs: Double-Strand Breaks; DDR: DNA Damage Response; EXO1: Exonuclease 1; FAS1/2: Fasciata1/2; FACT Facilitates Chromatin Transcription; FT: Flowering Locus T; GMI1: Gamma-Irradiation And Mitomycin C Induced 1; HAC1: Histone Acetyltransferase of the CBP Family 1; HAM1: Histone Acetyltransferase of the MYST Family 1; HAM2: Histone Acetyltransferase of the MYST Family 2; HAF1: Histone Acetyltransferase of the TAF Family 1; HAT: Histone Acetyl Transferase; HDA1: Histone Deacetylase 1; HDA6: Histone Deacetylase 6; HIRA Histone Regulatory Homolog A; HR- Homologous recombination; HAS: Helicase SANT Associated; HSS: HAND-SLANT-SLIDE; ICE1: Inducer of CBF Expression 1; INO80: Inositol Requiring Mutant 80; ISW1: Imitation Switch 1; KIN1/2: Kinase 1 /2; MET1: Methyltransferase 1; MET2: Methyltransferase 2; MINU MINUSCULE; MMS: Methyl Methane Sulfonate; MMS21: Methyl Methane Sulfonate Sensitivity 21; MRN: MRE11, RAD50 and NBS1; MSI1: Multicopy Suppressor Of Ira1; NAP1: Nucleosome Assembly Protein 1; NRP1/NRP2: NAP1-Related Protein; NER: Nucleotide Excision Repair; NHEJ Non-Homologous End Joining; PARP1: Poly-ADP Ribose Polymerase; PIE1: Photoperiod Independent Early Flowering 1; PIKK Phosphoinositide 3-Kinase-Like Kinase; PKL: PICKLE; PKR1/2: PICKLE Related 1/2; RAD: Radiation Sensitive Mutant; RD22: Responsive To Desiccation 22; RD29A: Responsive To Desiccation 29A; ROS: Reactive Oxygen Species; ROS1: Repressor of Silencing 1; RPA1E: Replication Protein A 1E; SANT Swi3, Ada2, N-Cor and TFIIIB; SEP3: SEPALLATA3; SCC3: Sister Chromatid Cohesion Protein 3; SMC1: Structural Maintenance of Chromosomes Protein 1; SMC3: Structural Maintenance of Chromosomes Protein 3; SOG1: Suppressor of Gamma Response 1; SWC6: SWR1 Complex Subunit 6; SWR1: SWI2/SNF2-Related 1; SYD: SPLAYED; SMC5: Structural Maintenance of Chromosome 5; SWI/SNF: Switch/Sucrose Non-Fermentable; TALENs: Transcription Activators Like Effector Nucleases; TRRAP Transformation/Transactivation Domain-Associated Protein; ZFNs: Zinc Finger Nucleases.
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The impact of oxidative stress damage induced by the environmental stressors on COVID-19.
Bakadia, BM, Boni, BOO, Ahmed, AAQ, Yang, G
Life sciences. 2021;:118653
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Abstract
The ongoing pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a substantial stressor that is greatly impacting environmental sustainability. Besides, the different pre-existing environmental stressors and coronavirus disease-2019 (COVID-19)-related stressors are further worsening the effects of the viral disease by inducing the generation of oxidative stress. The generated oxidative stress results in nucleic acid damage associated with viral mutations, that could potentially reduce the effectiveness of COVID-19 management, including the vaccine approach. The current review is aimed to overview the impact of the oxidative stress damage induced by various environmental stressors on COVID-19. The available data regarding the COVID-19-related stressors and the effects of oxidative stress damage induced by the chronic stress, exposure to free radicals, and malnutrition are also analyzed to showcase the promising options, which could be investigated further for sustainable control of the pandemic.
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Cellular pathologies and genotoxic effects arising secondary to heavy metal exposure: A review.
Kocadal, K, Alkas, FB, Battal, D, Saygi, S
Human & experimental toxicology. 2020;(1):3-13
Abstract
Environmental pollution is significant and oftentimes hazardous in the areas, where mining, foundries and smelters and other metallurgical operations are located. Systematic research on the chronic effects of metals started during the past century; nevertheless, it is evident that even today, there are large gaps in knowledge regarding the assessment of the health effects caused by environmental and occupational exposures to these metals. Heavy metals induce the production of reactive oxygen species (ROS) causing oxidative stress, make several repair-inhibiting cellular changes and alter the DNA repair processes. They favour the 'false' repairing of double-strand breaks (DSBs), propagate DNA mutations and induce carcinogenesis. A detailed literature search was performed using the MedLine/PubMed database. Depending on the mechanism of action, arsenicals can act as genotoxins, non-genotoxic agents and carcinogens. Cadmium can bind to proteins, reduce DNA repair, activate protein degradation, up-regulate cytokines and proto-oncogenes (c-fos, c-jun and c-myc), induce the expression of metallothionein, haeme-oxygenases, glutathione transferases, heat-shock proteins, acute-phase reactants and DNA polymerase β at lower concentrations. Inorganic mercury damages oxidative phosphorylation and electron transport pathways at the ubiquinone-cytochrome b5 locus and thus induces ROS production. Abandoned mining areas generate environmentally persistent waste. These specific sites urgently require maximally efficient and cheap remediation. This bears the need for methodologies employing green and sustainable remediation. Phytoremediation is important in that it is a prevalent in situ remediation technique. Its advantages include the use of solar energy, cost-effectiveness, easy operation, reduction in secondary contaminants, the use of biomass for biofuel production and low-cost adsorbents.
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Hydrogen peroxide, a potent inducer of global genomic instability.
Qi, L, Wu, XC, Zheng, DQ
Current genetics. 2019;(4):913-917
Abstract
Oxidative stress has been implicated in a variety of human diseases. One plausible mechanism is that reactive active species can induce DNA damages and jeopardize genome integrity. To explore how oxidative stress results in global genomic instability in cells, our current study examined the genomic alterations caused by H2O2 exposure at the whole genome level in yeast. Using SNP microarrays and genome sequencing, we mapped H2O2-induced genomic alterations in the yeast genome ranging from point mutations and mitotic recombination to chromosomal aneuploidy. Our results suggested most H2O2-induced mitotic recombination events were the result of DNA double-stand breaks generated by hydroxyl radicals. Moreover, the mutagenic effect of H2O2 was shown to be largely dependent on DNA polymerase ζ. Lastly, we showed that H2O2 exposure allows rapid phenotypic evolution in yeast strains. Our findings indicate DNA lesions resulting from H2O2 may be general factors that drive genome instability and phenotypic evolution in organisms.
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Sensitization of prostate cancer to radiation therapy: Molecules and pathways to target.
Yao, M, Rogers, L, Suchowerska, N, Choe, D, Al-Dabbas, MA, Narula, RS, Lyons, JG, Sved, P, Li, Z, Dong, Q
Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology. 2018;(2):283-300
Abstract
Radiation therapy is used to treat cancer by radiation-induced DNA damage. Despite the best efforts to eliminate cancer, some cancer cells survive irradiation, resulting in cancer progression or recurrence. Alteration in DNA damage repair pathways is common in cancers, resulting in modulation of their response to radiation. This article focuses on the recent findings about molecules and pathways that potentially can be targeted to sensitize prostate cancer cells to ionizing radiation, thereby achieving an improved therapeutic outcome.
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Translation acrobatics: how cancer cells exploit alternate modes of translational initiation.
Sriram, A, Bohlen, J, Teleman, AA
EMBO reports. 2018;(10)
Abstract
Recent work has brought to light many different mechanisms of translation initiation that function in cells in parallel to canonical cap-dependent initiation. This has important implications for cancer. Canonical cap-dependent translation initiation is inhibited by many stresses such as hypoxia, nutrient limitation, proteotoxic stress, or genotoxic stress. Since cancer cells are often exposed to these stresses, they rely on alternate modes of translation initiation for protein synthesis and cell growth. Cancer mutations are now being identified in components of the translation machinery and in cis-regulatory elements of mRNAs, which both control translation of cancer-relevant genes. In this review, we provide an overview on the various modes of non-canonical translation initiation, such as leaky scanning, translation re-initiation, ribosome shunting, IRES-dependent translation, and m6A-dependent translation, and then discuss the influence of stress on these different modes of translation. Finally, we present examples of how these modes of translation are dysregulated in cancer cells, allowing them to grow, to proliferate, and to survive, thereby highlighting the importance of translational control in cancer.
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7.
Photolyase: Dynamics and Mechanisms of Repair of Sun-Induced DNA Damage.
Zhang, M, Wang, L, Zhong, D
Photochemistry and photobiology. 2017;(1):78-92
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Abstract
Photolyase, a photomachine discovered half a century ago for repair of sun-induced DNA damage of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs), has been characterized extensively in biochemistry (function), structure and dynamics since 1980s. The molecular mechanism and repair photocycle have been revealed at the most fundamental level. Using femtosecond spectroscopy, we have mapped out the entire dynamical evolution and determined all actual timescales of the catalytic processes. Here, we review our recent efforts in studies of the dynamics of DNA repair by photolyases. The repair of CPDs in three life kingdoms includes seven electron transfer (ET) reactions among 10 elementary steps through initial bifurcating ET pathways, a direct tunneling route and a two-step hopping path both through an intervening adenine from the cofactor to CPD, with a conserved folded structure at the active site. The repair of 6-4PPs is challenging and requires similar ET reactions and a new cyclic proton transfer with a conserved histidine residue at the active site of (6-4) photolyases. Finally, we also summarize our efforts on multiple intraprotein ET of photolyases in different redox states and such mechanistic studies are critical to the functional mechanism of homologous cryptochromes of blue-light photoreceptors.
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How Trypanosoma cruzi deals with oxidative stress: Antioxidant defence and DNA repair pathways.
Machado-Silva, A, Cerqueira, PG, Grazielle-Silva, V, Gadelha, FR, Peloso, Ede F, Teixeira, SM, Machado, CR
Mutation research. Reviews in mutation research. 2016;:8-22
Abstract
Trypanosoma cruzi, the causative agent of Chagas disease, is an obligatory intracellular parasite with a digenetic life cycle. Due to the variety of host environments, it faces several sources of oxidative stress. In addition to reactive oxygen species (ROS) produced by its own metabolism, T. cruzi must deal with high ROS levels generated as part of the host's immune responses. Hence, the conclusion that T. cruzi has limited ability to deal with ROS (based on the lack of a few enzymes involved with oxidative stress responses) seems somewhat paradoxical. Actually, to withstand such variable sources of oxidative stress, T. cruzi has developed complex defence mechanisms. This includes ROS detoxification pathways that are distinct from the ones in the mammalian host, DNA repair pathways and specialized polymerases, which not only protect its genome from the resulting oxidative damage but also contribute to the generation of genetic diversity within the parasite population. Recent studies on T. cruzi's DNA repair pathways as mismatch repair (MMR) and GO system suggested that, besides a role associated with DNA repair, some proteins of these pathways may also be involved in signalling oxidative damage. Recent data also suggested that an oxidative environment might be beneficial for parasite survival within the host cell as it contributes to iron mobilization from the host's intracellular storages. Besides contributing to the understanding of basic aspects of T. cruzi biology, these studies are highly relevant since oxidative stress pathways are part of the poorly understood mechanisms behind the mode of action of drugs currently used against this parasite. By unveiling new peculiar aspects of T. cruzi biology, emerging data on DNA repair pathways and other antioxidant defences from this parasite have revealed potential new targets for a much needed boost in drug development efforts towards a better treatment for Chagas disease.
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Coffee Consumption and Oxidative Stress: A Review of Human Intervention Studies.
Martini, D, Del Bo', C, Tassotti, M, Riso, P, Del Rio, D, Brighenti, F, Porrini, M
Molecules (Basel, Switzerland). 2016;(8)
Abstract
Research on the potential protective effects of coffee and its bioactives (caffeine, chlorogenic acids and diterpenes) against oxidative stress and related chronic disease risk has been increasing in the last years. The present review summarizes the main findings on the effect of coffee consumption on protection against lipid, protein and DNA damage, as well as on the modulation of antioxidant capacity and antioxidant enzymes in human studies. Twenty-six dietary intervention studies (involving acute and chronic coffee intake) have been considered. Overall, the results suggest that coffee consumption can increase glutathione levels and improve protection against DNA damage, especially following regular/repeated intake. On the contrary, the effects of coffee on plasma antioxidant capacity and antioxidant enzymes, as well as on protein and lipid damage, are unclear following both acute and chronic exposure. The high heterogeneity in terms of type of coffee, doses and duration of the studies, the lack of information on coffee and/or brew bioactive composition, as well as the choice of biomarkers and the methods used for their evaluation, may partially explain the variability observed among findings. More robust and well-controlled intervention studies are necessary for a thorough understanding of the effect of coffee on oxidative stress markers in humans.
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DNA damage and the balance between survival and death in cancer biology.
Roos, WP, Thomas, AD, Kaina, B
Nature reviews. Cancer. 2016;(1):20-33
Abstract
DNA is vulnerable to damage resulting from endogenous metabolites, environmental and dietary carcinogens, some anti-inflammatory drugs, and genotoxic cancer therapeutics. Cells respond to DNA damage by activating complex signalling networks that decide cell fate, promoting not only DNA repair and survival but also cell death. The decision between cell survival and death following DNA damage rests on factors that are involved in DNA damage recognition, and DNA repair and damage tolerance, as well as on factors involved in the activation of apoptosis, necrosis, autophagy and senescence. The pathways that dictate cell fate are entwined and have key roles in cancer initiation and progression. Furthermore, they determine the outcome of cancer therapy with genotoxic drugs. Understanding the molecular basis of these pathways is important not only for gaining insight into carcinogenesis, but also in promoting successful cancer therapy. In this Review, we describe key decision-making nodes in the complex interplay between cell survival and death following DNA damage.