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DNA Repair

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https://www.readbyqxmd.com/read/28711786/exo1-suppresses-double-strand-break-induced-homologous-recombination-between-diverged-sequences-in-mammalian-cells
#1
Chun-Chin Chen, Elena Avdievich, Yongwei Zhang, Yu Zhang, Kaichun Wei, Kyeryoung Lee, Winfried Edelmann, Maria Jasin, Jeannine R LaRocque
DNA double-strand breaks (DSBs) can be repaired through several mechanisms, including homologous recombination (HR). While HR between identical sequences is robust in mammalian cells, HR between diverged sequences is suppressed by DNA mismatch-repair (MMR) components such as MSH2. Exonuclease I (EXO1) interacts with the MMR machinery and has been proposed to act downstream of the mismatch recognition proteins in mismatch correction. EXO1 has also been shown to participate in extensive DSB end resection, an initial step in the HR pathway...
July 10, 2017: DNA Repair
https://www.readbyqxmd.com/read/28719838/identification-of-a-prototypical-single-stranded-uracil-dna-glycosylase-from-listeria-innocua
#2
Jing Li, Ye Yang, Jose Guevara, Liangjiang Wang, Weiguo Cao
A recent phylogenetic study on UDG superfamily estimated a new clade of family 3 enzymes (SMUG1-like), which shares a lower homology with canonic SMUG1 enzymes. The enzymatic properties of the newly found putative DNA glycosylase are unknown. To test the potential UDG activity and evaluate phylogenetic classification, we isolated one SMUG1-like glycosylase representative from Listeria innocua (Lin). A biochemical screening of DNA glycosylase activity in vitro indicates that Lin SMUG1-like glycosylase is a single-strand selective uracil DNA glycosylase...
July 8, 2017: DNA Repair
https://www.readbyqxmd.com/read/28709015/human-cells-contain-a-factor-that-facilitates-the-dna-glycosylase-mediated-excision-of-oxidized-bases-from-occluded-sites-in-nucleosomes
#3
R L Maher, C G Marsden, A M Averill, S S Wallace, J B Sweasy, D S Pederson
Reactive oxygen species generate some 20,000 base lesions per human cell per day. The vast majority of these potentially mutagenic or cytotoxic lesions are subject to base excision repair (BER). Although chromatin remodelers have been shown to enhance the excision of oxidized bases from nucleosomes in vitro, it is not clear that they are recruited to and act at sites of BER in vivo. To test the hypothesis that cells possess factors that enhance BER in chromatin, we assessed the capacity of nuclear extracts from human cells to excise thymine glycol (Tg) lesions from exogenously added, model nucleosomes...
July 5, 2017: DNA Repair
https://www.readbyqxmd.com/read/28704715/differential-effect-of-the-overexpression-of-rad2-xpg-family-endonucleases-on-genome-integrity-in-yeast-and-human-cells
#4
Sonia Jimeno, Emilia Herrera-Moyano, Pedro Ortega, Andrés Aguilera
Eukaryotic cells possess several DNA endonucleases that are necessary to complete different steps in DNA metabolism. Rad2/XPG and Rad27/FEN1 belong to a group of evolutionary conserved proteins that constitute the Rad2 family. Given the important roles carried out by these nucleases in DNA repair and their capacity to create DNA breaks, we have investigated the effect that in vivo imbalance of these nucleases and others of the family have on genome integrity and cell proliferation. We show that overexpression of these nucleases causes genetic instability in both yeast and human cells...
July 3, 2017: DNA Repair
https://www.readbyqxmd.com/read/28704716/transcriptional-consequences-of-xpa-disruption-in-human-cell-lines
#5
Mandira Manandhar, Megan G Lowery, Karen S Boulware, Kevin H Lin, Yue Lu, Richard D Wood
Nucleotide excision repair (NER) in mammalian cells requires the xeroderma pigmentosum group A protein (XPA) as a core factor. Remarkably, XPA and other NER proteins have been detected by chromatin immunoprecipitation at some active promoters, and NER deficiency is reported to influence the activated transcription of selected genes. However, the global influence of XPA on transcription in human cells has not been determined. We analyzed the human transcriptome by RNA sequencing (RNA-Seq). We first confirmed that XPA is confined to the cell nucleus even in the absence of external DNA damage, in contrast to previous reports that XPA is normally resident in the cytoplasm and is imported following DNA damage...
June 29, 2017: DNA Repair
https://www.readbyqxmd.com/read/28689072/nucleolytic-degradation-of-3-ending-overhangs-is-essential-for-dna-end-resection-in-reca-loading-deficient-recb-mutants-of-escherichia-coli
#6
Siniša Ivanković, Dušica Vujaklija, Damir Đermić
Degradation of a 5'-ending strand is the hallmark of the universal process of DNA double strand break (DSB) resection, which results in creation of the central recombination intermediate, a 3'-ending overhang. Here we show that in Escherichia coli recB1080/recB1067 mutants, which are devoid of RecBCD's nuclease and RecA loading activities, degradation of the unwound 3' tail is as essential as is degradation of its 5'-ending complement. Namely, a synergistic action of ExoI, ExoVII, SbcCD and ExoX single-strand specific exonucleases (ssExos) of 3'-5' polarity was essential for preserving cell viability, DNA repair and homologous recombination in the recB1080/recB1067 mutants, to the same extent as the redundant action of 5'-tail trimming ssExos RecJ and ExoVII...
June 27, 2017: DNA Repair
https://www.readbyqxmd.com/read/28705538/cutting-edge-perspectives-in-genomic-maintenance-iv
#7
EDITORIAL
Philip C Hanawalt, Samuel H Wilson
No abstract text is available yet for this article.
June 24, 2017: DNA Repair
https://www.readbyqxmd.com/read/28688373/deletion-of-rd-ink4-arf-enhancer-a-novel-mutation-to-inactivate-the-ink4-arf-locus
#8
REVIEW
Ming J Poi, Thomas J Knobloch, Junan Li
The presence of an enhancer element, RD(INK4/ARF) (RD), in the prominent INK4-ARF locus provides a novel en bloc mechanism to simultaneously regulate the transcription of the p15(INK4B) (p15), p16(INK4A) (p16), and p14(ARF) tumor suppressor genes. While genetic inactivation of p15, p16, and p14(ARF) in human cancers has been extensively studied, little is known about RD alteration and its potential contributions to cancer progression. In this review, we discuss recent developments in RD alteration and its association with p15, p16, and p14(ARF) alterations in human cancers, and demonstrate that RD deletion may represent a novel mechanism to simultaneously down-regulate p15, p16, and p14(ARF), thus promoting carcinogenesis...
June 24, 2017: DNA Repair
https://www.readbyqxmd.com/read/28654806/ginger-extract-mitigates-ethanol-induced-changes-of-alpha-and-beta-myosin-heavy-chain-isoforms-gene-expression-and-oxidative-stress-in-the-heart-of-male-wistar-rats
#9
Alireza Shirpoor, Mitra Zerehpoosh, Mohammad Hasan Khadem Ansari, Fatemeh Kheradmand, Yousef Rasmi
The association between ethanol consumption and heart abnormalities, such as chamber dilation, myocyte damage, ventricular hypertrophy, and hypertension is well known. However, underlying molecular mediators involved in ethanol-induced heart abnormalities remain elusive. The aim of this study was to investigate the effect of chronic ethanol exposure on alpha and beta - myosin heavy chain (MHC) isoforms gene expression transition and oxidative stress in rats' heart. It was also planned to find out whether ginger extract mitigated the abnormalities induced by ethanol in rats' heart...
June 21, 2017: DNA Repair
https://www.readbyqxmd.com/read/28648892/asciz-atmin-is-dispensable-for-atm-signaling-in-response-to-replication-stress
#10
Rui Liu, Ashleigh King, Nicolas C Hoch, Catherine Chang, Gemma L Kelly, Andrew J Deans, Jörg Heierhorst
The ATM kinase plays critical roles in the response to DNA double-strand breaks, and can also be activated by prolonged DNA replication blocks. It has recently been proposed that replication stress-dependent ATM activation is mediated by ASCIZ (also known as ATMIN, ZNF822), an essential developmental transcription factor. In contrast, we show here that ATM activation, and phosphorylation of its substrates KAP1, p53 and H2AX in response to the replication blocking agent aphidicolin was unaffected in both immortalized and primary ASCIZ/ATMIN-deficient murine embryonic fibroblasts compared to control cells...
June 17, 2017: DNA Repair
https://www.readbyqxmd.com/read/28641943/template-switching-during-replication-fork-repair-in-bacteria
#11
REVIEW
Susan T Lovett
Replication forks frequently are challenged by lesions on the DNA template, replication-impeding DNA secondary structures, tightly bound proteins or nucleotide pool imbalance. Studies in bacteria have suggested that under these circumstances the fork may leave behind single-strand DNA gaps that are subsequently filled by homologous recombination, translesion DNA synthesis or template-switching repair synthesis. This review focuses on the template-switching pathways and how the mechanisms of these processes have been deduced from biochemical and genetic studies...
June 13, 2017: DNA Repair
https://www.readbyqxmd.com/read/28651167/error-prone-bypass-of-o-6-methylguanine-by-dna-polymerase-of-pseudomonas-aeruginosa-phage-pap1
#12
Shiling Gu, Jingyuan Xiong, Ying Shi, Jia You, Zhenyu Zou, Xiaoying Liu, Huidong Zhang
O(6)-Methylguanine (O(6)-MeG) is highly mutagenic and is commonly found in DNA exposed to methylating agents, generally leads to G:C to A:T mutagenesis. To study DNA replication encountering O(6)-MeG by the DNA polymerase (gp90) of P. aeruginosa phage PaP1, we analyzed steady-state and pre-steady-state kinetics of nucleotide incorporation opposite O(6)-MeG by gp90 exo(-). O(6)-MeG partially inhibited full-length extension by gp90 exo(-). O(6)-MeG greatly reduces dNTP incorporation efficiency, resulting in 67-fold preferential error-prone incorporation of dTTP than dCTP...
June 10, 2017: DNA Repair
https://www.readbyqxmd.com/read/28623093/the-role-of-smarcal1-in-replication-fork-stability-and-telomere-maintenance
#13
REVIEW
Natalia Lugli, Sotirios K Sotiriou, Thanos D Halazonetis
SMARCAL1 (SWI/SNF Related, Matrix Associated, Actin Dependent Regulator Of Chromatin, Subfamily A-Like 1), also known as HARP, is an ATP-dependent annealing helicase that stabilizes replication forks during DNA damage. Mutations in this gene are the cause of Schimke immune-osseous dysplasia (SIOD), an autosomal recessive disorder characterized by T-cell immunodeficiency and growth dysfunctions. In this review, we summarize the main roles of SMARCAL1 in DNA repair, telomere maintenance and replication fork stability in response to DNA replication stress...
June 10, 2017: DNA Repair
https://www.readbyqxmd.com/read/28690053/close-encounters-moving-along-bumps-breaks-and-bubbles-on-expanded-trinucleotide-tracts
#14
REVIEW
Aris A Polyzos, Cynthia T McMurray
Expansion of simple triplet repeats (TNR) underlies more than 30 severe degenerative diseases. There is a good understanding of the major pathways generating an expansion, and the associated polymerases that operate during gap filling synthesis at these "difficult to copy" sequences. However, the mechanism by which a TNR is repaired depends on the type of lesion, the structural features imposed by the lesion, the assembled replication/repair complex, and the polymerase that encounters it. The relationships among these parameters are exceptionally complex and how they direct pathway choice is poorly understood...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28687338/replicative-dna-polymerase-defects-in-human-cancers-consequences-mechanisms-and-implications-for-therapy
#15
REVIEW
Stephanie R Barbari, Polina V Shcherbakova
The fidelity of DNA replication relies on three error avoidance mechanisms acting in series: nucleotide selectivity of replicative DNA polymerases, exonucleolytic proofreading, and post-replicative DNA mismatch repair (MMR). MMR defects are well known to be associated with increased cancer incidence. Due to advances in DNA sequencing technologies, the past several years have witnessed a long-predicted discovery of replicative DNA polymerase defects in sporadic and hereditary human cancers. The polymerase mutations preferentially affect conserved amino acid residues in the exonuclease domain and occur in tumors with an extremely high mutation load...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28663070/poetry-in-motion-increased-chromosomal-mobility-after-dna-damage
#16
REVIEW
Michael J Smith, Rodney Rothstein
Double-strand breaks (DSBs) are among the most lethal DNA lesions, and a variety of pathways have evolved to manage their repair in a timely fashion. One such pathway is homologous recombination (HR), in which information from an undamaged donor site is used as a template for repair. Although many of the biochemical steps of HR are known, the physical movements of chromosomes that must underlie the pairing of homologous sequence during mitotic DSB repair have remained mysterious. Recently, several groups have begun to use a variety of genetic and cell biological tools to study this important question...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28652129/evolutionary-dynamics-and-significance-of-multiple-subclonal-mutations-in-cancer
#17
REVIEW
Robert A Beckman, Lawrence A Loeb
For the last 40 years the authors have collaborated on trying to understand the complexities of human cancer by formulating testable mathematical models that are based on mutation accumulation in human malignancies. We summarize the concepts encompassed by multiple mutations in human cancers in the context of source, accumulation during carcinogenesis and tumor progression, and therapeutic consequences. We conclude that the efficacious treatment of human cancer by targeted therapy will involve individualized, uniquely directed specific agents singly and in simultaneous combinations, and take into account the importance of targeting resistant subclonal mutations, particularly those subclones with alterations in DNA repair genes, DNA polymerase, and other genes required to maintain genetic stability...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28641942/the-top1-paradox-friend-and-foe-of-the-eukaryotic-genome
#18
REVIEW
Nayun Kim, Sue Jinks-Robertson
Topoisomerases manage the torsional stress associated with the separation of DNA strands during transcription and DNA replication. Eukaryotic Topoisomerase I (Top1) is a Type IB enzyme that nicks and rejoins only one strand of duplex DNA, and it is especially important during transcription. By resolving transcription-associated torsional stress, Top1 reduces the accumulation of genome-destabilizing R-loops and non-B DNA structures. The DNA nicking activity of Top1, however, can also initiate genome instability in the form of illegitimate recombination, homologous recombination and mutagenesis...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28641941/role-of-recombination-and-replication-fork-restart-in-repeat-instability
#19
REVIEW
Erica J Polleys, Nealia C M House, Catherine H Freudenreich
Eukaryotic genomes contain many repetitive DNA sequences that exhibit size instability. Some repeat elements have the added complication of being able to form secondary structures, such as hairpin loops, slipped DNA, triplex DNA or G-quadruplexes. Especially when repeat sequences are long, these DNA structures can form a significant impediment to DNA replication and repair, leading to DNA nicks, gaps, and breaks. In turn, repair or replication fork restart attempts within the repeat DNA can lead to addition or removal of repeat elements, which can sometimes lead to disease...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28641940/dormant-origins-as-a-built-in-safeguard-in-eukaryotic-dna-replication-against-genome-instability-and-disease-development
#20
REVIEW
Naoko Shima, Kayla D Pederson
DNA replication is a prerequisite for cell proliferation, yet it can be increasingly challenging for a eukaryotic cell to faithfully duplicate its genome as its size and complexity expands. Dormant origins now emerge as a key component for cells to successfully accomplish such a demanding but essential task. In this perspective, we will first provide an overview of the fundamental processes eukaryotic cells have developed to regulate origin licensing and firing. With a special focus on mammalian systems, we will then highlight the role of dormant origins in preventing replication-associated genome instability and their functional interplay with proteins involved in the DNA damage repair response for tumor suppression...
June 9, 2017: DNA Repair
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