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https://www.readbyqxmd.com/read/29176630/break-induced-replication-promotes-formation-of-lethal-joint-molecules-dissolved-by-srs2
#1
Rajula Elango, Ziwei Sheng, Jessica Jackson, Jenna DeCata, Younis Ibrahim, Nhung T Pham, Diana H Liang, Cynthia J Sakofsky, Alessandro Vindigni, Kirill S Lobachev, Grzegorz Ira, Anna Malkova
Break-induced replication (BIR) is a DNA double-strand break repair pathway that leads to genomic instabilities similar to those observed in cancer. BIR proceeds by a migrating bubble where asynchrony between leading and lagging strand synthesis leads to accumulation of long single-stranded DNA (ssDNA). It remains unknown how this ssDNA is prevented from unscheduled pairing with the template, which can lead to genomic instability. Here, we propose that uncontrolled Rad51 binding to this ssDNA promotes formation of toxic joint molecules that are counteracted by Srs2...
November 27, 2017: Nature Communications
https://www.readbyqxmd.com/read/29072253/corrigendum-mus81-nuclease-activity-is-essential-for-replication-stress-tolerance-and-chromosome-segregation-in-brca2-deficient-cells
#2
Xianning Lai, Ronan Broderick, Valérie Bergoglio, Jutta Zimmer, Sophie Badie, Wojciech Niedzwiedz, Jean-Sébastien Hoffmann, Madalena Tarsounas
This corrects the article DOI: 10.1038/ncomms15983.
October 26, 2017: Nature Communications
https://www.readbyqxmd.com/read/29038425/mre11-and-exo1-nucleases-degrade-reversed-forks-and-elicit-mus81-dependent-fork-rescue-in-brca2-deficient-cells
#3
Delphine Lemaçon, Jessica Jackson, Annabel Quinet, Joshua R Brickner, Shan Li, Stephanie Yazinski, Zhongsheng You, Grzegorz Ira, Lee Zou, Nima Mosammaparast, Alessandro Vindigni
The breast cancer susceptibility proteins BRCA1 and BRCA2 have emerged as key stabilizing factors for the maintenance of replication fork integrity following replication stress. In their absence, stalled replication forks are extensively degraded by the MRE11 nuclease, leading to chemotherapeutic sensitivity. Here we report that BRCA proteins prevent nucleolytic degradation by protecting replication forks that have undergone fork reversal upon drug treatment. The unprotected regressed arms of reversed forks are the entry point for MRE11 in BRCA-deficient cells...
October 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/29035360/ezh2-promotes-degradation-of-stalled-replication-forks-by-recruiting-mus81-through-histone-h3-trimethylation
#4
Beatrice Rondinelli, Ewa Gogola, Hatice Yücel, Alexandra A Duarte, Marieke van de Ven, Roxanne van der Sluijs, Panagiotis A Konstantinopoulos, Jos Jonkers, Raphaël Ceccaldi, Sven Rottenberg, Alan D D'Andrea
The emergence of resistance to poly-ADP-ribose polymerase inhibitors (PARPi) poses a threat to the treatment of BRCA1 and BRCA2 (BRCA1/2)-deficient tumours. Stabilization of stalled DNA replication forks is a recently identified PARPi-resistance mechanism that promotes genomic stability in BRCA1/2-deficient cancers. Dissecting the molecular pathways controlling genomic stability at stalled forks is critical. Here we show that EZH2 localizes at stalled forks where it methylates Lys27 on histone 3 (H3K27me3), mediating recruitment of the MUS81 nuclease...
November 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28988007/chromosome-copy-number-variation-in-telomerized-human-bone-marrow-stromal-cells-insights-for-monitoring-safe-ex-vivo-expansion-of-adult-stem-cells
#5
Jorge S Burns, Linda Harkness, Abdullah Aldahmash, Laurent Gautier, Moustapha Kassem
Adult human bone marrow stromal cells (hBMSC) cultured for cell therapy require evaluation of potency and stability for safe use. Chromosomal aberrations upsetting genomic integrity in such cells have been contrastingly described as "Limited" or "Significant". Previously reported stepwise acquisition of a spontaneous neoplastic phenotype during three-year continuous culture of telomerized cells (hBMSC-TERT20) didn't alter a diploid karyotype measured by spectral karyotype analysis (SKY). Such screening may not adequately monitor abnormal and potentially tumorigenic hBMSC in clinical scenarios...
September 25, 2017: Stem Cell Research
https://www.readbyqxmd.com/read/28969641/role-of-pcna-and-rfc-in-promoting-mus81-complex-activity
#6
Alexandra Sisakova, Veronika Altmannova, Marek Sebesta, Lumir Krejci
BACKGROUND: Proper DNA replication is essential for faithful transmission of the genome. However, replication stress has serious impact on the integrity of the cell, leading to stalling or collapse of replication forks, and has been determined as a driving force of carcinogenesis. Mus81-Mms4 complex is a structure-specific endonuclease previously shown to be involved in processing of aberrant replication intermediates and promotes POLD3-dependent DNA synthesis via break-induced replication...
October 2, 2017: BMC Biology
https://www.readbyqxmd.com/read/28922417/lingering-single-strand-breaks-trigger-rad51-independent-homology-directed-repair-of-collapsed-replication-forks-in-the-polynucleotide-kinase-phosphatase-mutant-of-fission-yeast
#7
Arancha Sanchez, Mariana C Gadaleta, Oliver Limbo, Paul Russell
The DNA repair enzyme polynucleotide kinase/phosphatase (PNKP) protects genome integrity by restoring ligatable 5'-phosphate and 3'-hydroxyl termini at single-strand breaks (SSBs). In humans, PNKP mutations underlie the neurological disease known as MCSZ, but these individuals are not predisposed for cancer, implying effective alternative repair pathways in dividing cells. Homology-directed repair (HDR) of collapsed replication forks was proposed to repair SSBs in PNKP-deficient cells, but the critical HDR protein Rad51 is not required in PNKP-null (pnk1Δ) cells of Schizosaccharomyces pombe...
September 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28813668/subnuclear-relocalization-of-structure-specific-endonucleases-in-response-to-dna-damage
#8
Irene Saugar, Alberto Jiménez-Martín, José Antonio Tercero
Structure-specific endonucleases contribute to the maintenance of genome integrity by cleaving DNA intermediates that need to be resolved for faithful DNA repair, replication, or recombination. Despite advances in the understanding of their function and regulation, it is less clear how these proteins respond to genotoxic stress. Here, we show that the structure-specific endonuclease Mus81-Mms4/EME1 relocalizes to subnuclear foci following DNA damage and colocalizes with the endonucleases Rad1-Rad10 (XPF-ERCC1) and Slx1-Slx4...
August 15, 2017: Cell Reports
https://www.readbyqxmd.com/read/28781165/multi-invasions-are-recombination-byproducts-that-induce-chromosomal-rearrangements
#9
Aurèle Piazza, William Douglass Wright, Wolf-Dietrich Heyer
Inaccurate repair of broken chromosomes generates structural variants that can fuel evolution and inflict pathology. We describe a novel rearrangement mechanism in which translocation between intact chromosomes is induced by a lesion on a third chromosome. This multi-invasion-induced rearrangement (MIR) stems from a homologous recombination byproduct, where a broken DNA end simultaneously invades two intact donors. No homology is required between the donors, and the intervening sequence from the invading molecule is inserted at the translocation site...
August 10, 2017: Cell
https://www.readbyqxmd.com/read/28714477/mus81-nuclease-activity-is-essential-for-replication-stress-tolerance-and-chromosome-segregation-in-brca2-deficient-cells
#10
Xianning Lai, Ronan Broderick, Valérie Bergoglio, Jutta Zimmer, Sophie Badie, Wojciech Niedzwiedz, Jean-Sébastien Hoffmann, Madalena Tarsounas
Failure to restart replication forks stalled at genomic regions that are difficult to replicate or contain endogenous DNA lesions is a hallmark of BRCA2 deficiency. The nucleolytic activity of MUS81 endonuclease is required for replication fork restart under replication stress elicited by exogenous treatments. Here we investigate whether MUS81 could similarly facilitate DNA replication in the context of BRCA2 abrogation. Our results demonstrate that replication fork progression in BRCA2-deficient cells requires MUS81...
July 17, 2017: Nature Communications
https://www.readbyqxmd.com/read/28645372/analysis-of-structure-selective-endonuclease-activities-from-yeast-and-human-extracts
#11
Joao Matos, Stephen C West
The efficient separation of two equal DNA masses to the daughter cells is an essential step in mitosis. This process is dependent upon the removal of any remaining recombination or replication intermediates that link sister chromatids, and a failure to resolve these intermediates leads to genome instability. Similarly, a failure to resolve meiotic recombination intermediates that link homologous chromosomes can cause chromosome nondisjunction and aneuploidy. Cleavage of these potentially toxic replication/recombination intermediates requires the Mus81 endonuclease, which is active upon flaps, forks, and more complex secondary structures in DNA such as Holliday junctions...
2017: Methods in Enzymology
https://www.readbyqxmd.com/read/28640495/control-of-mus81-nuclease-during-the-cell-cycle
#12
REVIEW
Boris Pfander, Joao Matos
DNA replication and homologous recombination involve the formation of branched DNA structures that physically link chromosomes. Such DNA-based connections, which arise during S-phase, are typically disengaged prior to entry into mitosis, in order to ensure proper chromosome segregation. Exceptions can, however, occur: replication stress, or elevated levels of DNA damage, may cause cells to enter mitosis with unfinished replication as well as carrying recombination intermediates, such as Holliday junctions. Hence, cells are equipped with pathways that recognize and process branched DNA structures, and evolved mechanisms to enhance their function when on the verge of undergoing cell division...
July 2017: FEBS Letters
https://www.readbyqxmd.com/read/28586299/inter-fork-strand-annealing-causes-genomic-deletions-during-the-termination-of-dna-replication
#13
Carl A Morrow, Michael O Nguyen, Andrew Fower, Io Nam Wong, Fekret Osman, Claire Bryer, Matthew C Whitby
Problems that arise during DNA replication can drive genomic alterations that are instrumental in the development of cancers and many human genetic disorders. Replication fork barriers are a commonly encountered problem, which can cause fork collapse and act as hotspots for replication termination. Collapsed forks can be rescued by homologous recombination, which restarts replication. However, replication restart is relatively slow and, therefore, replication termination may frequently occur by an active fork converging on a collapsed fork...
June 6, 2017: ELife
https://www.readbyqxmd.com/read/28575661/recq5-helicase-cooperates-with-mus81-endonuclease-in-processing-stalled-replication-forks-at-common-fragile-sites-during-mitosis
#14
Stefano Di Marco, Zdenka Hasanova, Radhakrishnan Kanagaraj, Nagaraja Chappidi, Veronika Altmannova, Shruti Menon, Hana Sedlackova, Jana Langhoff, Kalpana Surendranath, Daniela Hühn, Rahul Bhowmick, Victoria Marini, Stefano Ferrari, Ian D Hickson, Lumir Krejci, Pavel Janscak
The MUS81-EME1 endonuclease cleaves late replication intermediates at common fragile sites (CFSs) during early mitosis to trigger DNA-repair synthesis that ensures faithful chromosome segregation. Here, we show that these DNA transactions are promoted by RECQ5 DNA helicase in a manner dependent on its Ser727 phosphorylation by CDK1. Upon replication stress, RECQ5 associates with CFSs in early mitosis through its physical interaction with MUS81 and promotes MUS81-dependent mitotic DNA synthesis. RECQ5 depletion or mutational inactivation of its ATP-binding site, RAD51-interacting domain, or phosphorylation site causes excessive binding of RAD51 to CFS loci and impairs CFS expression...
June 1, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28512214/correction-for-mu%C3%A3-oz-galv%C3%A3-n-et-al-distinct-roles-of-mus81-yen1-slx1-slx4-and-rad1-nucleases-in-the-repair-of-replication-born-double-strand-breaks-by-sister-chromatid-exchange
#15
Sandra Muñoz-Galván, Cristina Tous, Miguel G Blanco, Erin K Schwartz, Kirk T Ehmsen, Stephen C West, Wolf-Dietrich Heyer, Andrés Aguilera
No abstract text is available yet for this article.
June 1, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28510302/association-study-of-genetic-variation-in-dna-repair-pathway-genes-and-risk-of-basal-cell-carcinoma
#16
Yuan Lin, Harvind S Chahal, Wenting Wu, Hyunje G Cho, Katherine J Ransohoff, Fengju Song, Jean Y Tang, Kavita Y Sarin, Jiali Han
DNA repair plays a critical role in protecting the genome from ultraviolet radiation and maintaining the genomic integrity of cells. Genetic variants in DNA repair-related genes can influence an individual's DNA repair capacity, which may be related to the risk of developing basal cell carcinoma (BCC). We comprehensively assessed the associations of 2,965 independent single-nucleotide polymorphisms (SNPs) across 165 DNA repair pathway genes with BCC risk in a genome-wide association meta-analysis totaling 17,187 BCC cases and 287,054 controls from two data sets...
September 1, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28509359/the-dna-translocase-rad5a-acts-independently-of-the-other-main-dna-repair-pathways-and-requires-both-its-atpase-and-ring-domain-for-activity-in-arabidopsis-thaliana
#17
Tobias Klemm, Anja Mannuß, Daniela Kobbe, Alexander Knoll, Oliver Trapp, Annika Dorn, Holger Puchta
Multiple pathways exist to repair DNA damage induced by methylating and crosslinking agents in Arabidopsis thaliana. The SWI2/SNF2 translocase RAD5A, the functional homolog of budding yeast Rad5 that is required for the error-free branch of post-replicative repair, plays a surprisingly prominent role in the repair of both kinds of lesions in Arabidopsis. Here we show that both the ATPase domain and the ubiquitination function of the RING domain of the Arabidopsis protein are essential for the cellular response to different forms of DNA damage...
August 2017: Plant Journal: for Cell and Molecular Biology
https://www.readbyqxmd.com/read/28369583/substrate-preference-of-gen-endonucleases-highlights-the-importance-of-branched-structures-as-dna-damage-repair-intermediates
#18
Stephanie P Bellendir, Danielle J Rognstad, Lydia P Morris, Grzegorz Zapotoczny, William G Walton, Matthew R Redinbo, Dale A Ramsden, Jeff Sekelsky, Dorothy A Erie
Human GEN1 and yeast Yen1 are endonucleases with the ability to cleave Holliday junctions (HJs), which are proposed intermediates in recombination. In vivo, GEN1 and Yen1 function secondarily to Mus81, which has weak activity on intact HJs. We show that the genetic relationship is reversed in Drosophila, with Gen mutants having more severe defects than mus81 mutants. In vitro, DmGen, like HsGEN1, efficiently cleaves HJs, 5΄ flaps, splayed arms, and replication fork structures. We find that the cleavage rates for 5΄ flaps are significantly higher than those for HJs for both DmGen and HsGEN1, even in vast excess of enzyme over substrate...
May 19, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/28341648/dna-damage-tolerance-pathway-choice-through-uls1-modulation-of-srs2-sumoylation-in-saccharomyces-cerevisiae
#19
Karol Kramarz, Seweryn Mucha, Ireneusz Litwin, Anna Barg-Wojas, Robert Wysocki, Dorota Dziadkowiec
DNA damage tolerance and homologous recombination pathways function to bypass replication-blocking lesions and ensure completion of DNA replication. However, inappropriate activation of these pathways may lead to increased mutagenesis or formation of deleterious recombination intermediates, often leading to cell death or cancer formation in higher organisms. Post-translational modifications of PCNA regulate the choice of repair pathways at replication forks. Its monoubiquitination favors translesion synthesis, while polyubiquitination stimulates template switching...
May 2017: Genetics
https://www.readbyqxmd.com/read/28327556/control-of-structure-specific-endonucleases-to-maintain-genome-stability
#20
REVIEW
Pierre-Marie Dehé, Pierre-Henri L Gaillard
Structure-specific endonucleases (SSEs) have key roles in DNA replication, recombination and repair, and emerging roles in transcription. These enzymes have specificity for DNA secondary structure rather than for sequence, and therefore their activity must be precisely controlled to ensure genome stability. In this Review, we discuss how SSEs are controlled as part of genome maintenance pathways in eukaryotes, with an emphasis on the elaborate mechanisms that regulate the members of the major SSE families - including the xeroderma pigmentosum group F-complementing protein (XPF) and MMS and UV-sensitive protein 81 (MUS81)-dependent nucleases, and the flap endonuclease 1 (FEN1), XPG and XPG-like endonuclease 1 (GEN1) enzymes - during processes such as DNA adduct repair, Holliday junction processing and replication stress...
May 2017: Nature Reviews. Molecular Cell Biology
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