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Elegans dna damage

Peter Sykora, Ylenia Chiari, Andrew Heaton, Nickolas Moreno, Scott Glaberman, Robert W Sobol
DNA damage has been linked to genomic instability and the progressive breakdown of cellular and organismal homeostasis, leading to the onset of disease and reduced longevity. Insults to DNA from endogenous sources include base deamination, base hydrolysis, base alkylation, and metabolism-induced oxidative damage that can lead to single-strand and double-strand DNA breaks. Alternatively, exposure to environmental pollutants, radiation or ultra-violet light, can also contribute to exogenously derived DNA damage...
March 14, 2018: Environmental and Molecular Mutagenesis
Alexey Moskalev, Mikhail Shaposhnikov, Nadezhda Zemskaya, Alexey Belyi, Eugenia Dobrovolskaya, Anna Patova, Zulfiya Guvatova, Elena Lukyanova, Anastasiya Snezhkina, Anna Kudryavtseva
BACKGROUND: We have previously showed that the carotenoid fucoxanthin can increase the lifespan in Drosophila melanogaster and Caenorhabditis elegans. However, the molecular mechanisms of the geroprotective effect of fucoxanthin have not been studied so far. RESULTS: Here, we studied the effects of fucoxanthin on the Drosophila aging process at the molecular and the whole organism levels. At the organismal level, fucoxanthin increased the median lifespan and had a positive effect on fecundity, fertility, intestinal barrier function, and nighttime sleep...
February 9, 2018: BMC Genomics
Toshia R Myers, Pier Giorgio Amendola, Yvonne C Lussi, Anna Elisabetta Salcini
Post-translational modifications of histones, constitutive components of chromatin, regulate chromatin compaction and control all DNA-based cellular processes. C. elegans JMJD-1.2, a member of the KDM7 family, is a demethylase active towards several lysine residues on Histone 3 (H3), but its contribution in regulating histone methylation in germ cells has not been fully investigated. Here, we show that jmjd-1.2 is expressed abundantly in the germline where it controls the level of histone 3 lysine 9, lysine 23 and lysine 27 di-methylation (H3K9/K23/K27me2) both in mitotic and meiotic cells...
February 28, 2018: Scientific Reports
Silvana Rošić, Rachel Amouroux, Cristina E Requena, Ana Gomes, Max Emperle, Toni Beltran, Jayant K Rane, Sarah Linnett, Murray E Selkirk, Philipp H Schiffer, Allison J Bancroft, Richard K Grencis, Albert Jeltsch, Petra Hajkova, Peter Sarkies
Methylation at the 5 position of cytosine in DNA (5meC) is a key epigenetic mark in eukaryotes. Once introduced, 5meC can be maintained through DNA replication by the activity of 'maintenance' DNA methyltransferases (DNMTs). Despite their ancient origin, DNA methylation pathways differ widely across animals, such that 5meC is either confined to transcribed genes or lost altogether in several lineages. We used comparative epigenomics to investigate the evolution of DNA methylation. Although the model nematode Caenorhabditis elegans lacks DNA methylation, more basal nematodes retain cytosine DNA methylation, which is targeted to repeat loci...
February 19, 2018: Nature Genetics
Christin Riedinger, Michael Mendler, Andrea Schlotterer, Thomas Fleming, Jürgen Okun, Hans-Peter Hammes, Stephan Herzig, Peter P Nawroth
The enzyme AICAR-transformylase/IMP cyclohydrolase (ATIC) catalyzes the last two steps of purine de-novo synthesis. It metabolizes AICAR, which is an AMP analogue, leading to activation of AMPK. It was investigated whether the AICAR-ATIC pathway plays a role in the high glucose (HG) mediated DNA damage response and AICAR mediated AMPK activation, explaining the detrimental effects of glucose on neuronal damages and shortening of lifespan. HG up-regulated the expression and activity of Caenorhabditis elegans homologue of ATIC, C55F2...
February 2, 2018: Journal of Biological Chemistry
Liangwen Chen, Huangqi Tang, Yan Du, Zhangyu Dai, Ting Wang, Lijun Wu, Libin Zhou, Po Bian
Heavy-ion radiation has attracted extensive attention as an effective cancer therapy because of the varying energy deposition along its track and its high cell-killing effect. Reproductive cell death (RCD), also known as clonogenic death, is an important mode of death of the cancer cells after radiotherapy. Although RCD induced by heavy-ion irradiation with various linear energy transfers has been demonstrated using clonogenic assay in vitro, little is known about the distribution of RCD across the range of heavy-ion irradiation at the level of whole organisms...
February 1, 2018: DNA Repair
Dayana R D'Amora, Queenie Hu, Monica Pizzardi, Terrance J Kubiseski
As part of the DNA damage response (DDR) network, the tumour suppressor Breast cancer susceptibility gene 1 (BRCA1) is activated to facilitate DNA repair, transcription and cell cycle control. BRC-1, the Caenorhabditis elegans ortholog of BRCA1, has conserved function in DNA double strand break repair, wherein a loss of brc-1 results in high levels of germline apoptosis. BRAP2/IMP was initially identified as a BRCA1 associated binding protein and previously we have shown that the C. elegans brap-2 deletion mutant experiences BRC-1 dependent larval arrest when exposed to low concentrations of paraquat...
January 22, 2018: Cell Death and Differentiation
Krzysztof Drabikowski, Jacqueline Ferralli, Michal Kistowski, Jacek Oledzki, Michal Dadlez, Ruth Chiquet-Ehrismann
Post-translational modification by small ubiquitin-related modifier (SUMO) is a key regulator of cell physiology, modulating protein-protein and protein-DNA interactions. Recently, SUMO modifications were postulated to be involved in response to various stress stimuli. We aimed to identify the near complete set of proteins modified by SUMO and the dynamics of the modification in stress conditions in the higher eukaryote, Caenorhabditis elegans. We identified 874 proteins modified by SUMO in the worm. We have analyzed the SUMO modification in stress conditions including heat shock, DNA damage, arsenite induced cellular stress, ER and osmotic stress...
January 18, 2018: Scientific Reports
Henok Kassahun, Tanima SenGupta, Alfonso Schiavi, Silvia Maglioni, Hanne K Skjeldam, Katarzyna Arczewska, Nicole L Brockway, Suzanne Estes, Lars Eide, Natascia Ventura, Hilde Nilsen
Oxidation of DNA bases, an inevitable consequence of oxidative stress, requires the base excision repair (BER) pathway for repair. Caenorhabditis elegans is a well-established model to study phenotypic consequences and cellular responses to oxidative stress. To better understand how BER affects phenotypes associated with oxidative stress, we characterised the C. elegans nth-1 mutant, which lack the only DNA glycosylase dedicated to repair of oxidative DNA base damage, the NTH-1 DNA glycosylase. We show that nth-1 mutants have mitochondrial dysfunction characterised by lower mitochondrial DNA copy number, reduced mitochondrial membrane potential, and increased steady-state levels of reactive oxygen species...
January 2018: DNA Repair
Simone Bertolini, Bin Wang, Bettina Meier, Ye Hong, Anton Gartner
Relatively little is known about the cross-talk between the spindle assembly checkpoint and the DNA damage response, especially in multicellular organisms. We performed a Caenorhabditis elegans forward genetic screen to uncover new genes involved in the repair of DNA damage induced by ionizing radiation. We isolated a mutation, gt2000 , which confers hypersensitivity to ionizing radiation and showed that gt2000 introduces a premature stop in bub-3 BUB-3 is a key component of the spindle assembly checkpoint...
December 4, 2017: G3: Genes—Genomes—Genetics
Qingqing Li, Jue Shi, Lianyun Chen, Furu Zhan, Hang Yuan, Jun Wang, An Xu, Lijun Wu
Though the signaling events involved in radiation induced bystander effects (RIBE) have been investigated both in vitro and in vivo, the spatial function of these communications, especially the related signaling pathways, is not fully elucidated. In the current study, significant increases of DNA damage were clearly observed in C. elegans germline upon irradiation to both intra-system of posterior pharynx and inter-system of vulva, in which more severe damage, even to F1 generation worms, was shown for vulva irradiation...
August 1, 2017: Oncotarget
Diletta Edifizi, Hendrik Nolte, Vipin Babu, Laia Castells-Roca, Michael M Mueller, Susanne Brodesser, Marcus Krüger, Björn Schumacher
DNA damage causally contributes to aging and age-related diseases. Mutations in nucleotide excision repair (NER) genes cause highly complex congenital syndromes characterized by growth retardation, cancer susceptibility, and accelerated aging in humans. Orthologous mutations in Caenorhabditis elegans lead to growth delay, genome instability, and accelerated functional decline, thus allowing investigation of the consequences of persistent DNA damage during development and aging in a simple metazoan model. Here, we conducted proteome, lipidome, and phosphoproteome analysis of NER-deficient animals in response to UV treatment to gain comprehensive insights into the full range of physiological adaptations to unrepaired DNA damage...
August 29, 2017: Cell Reports
Dong Lin, Reza Izadpanah, Stephen E Braun, Eckhard Alt
BRCA1 plays a central role in DNA repair. Although N-terminal RING and C-terminal BRCT domains are studied well, the functions of the central region of BRCA1 are poorly characterized. Here, we report a structural and functional analysis of BRCA1 alleles and functional human BRCA1 in chicken B-lymphocyte cell line DT40. The combination of "homologous recombineering" and "RT-cassette" enables modifications of chicken BRCA1 gene in Escherichia coli. Mutant BRCA1 knock-in DT40 cell lines were generated using BRCA1 mutation constructs by homologous recombination with a targeting efficiency of up to 100%...
August 18, 2017: Cell Biology International
Talia Hatkevich, Jeff Sekelsky
The functions of the Bloom syndrome helicase (BLM) and its orthologs are well characterized in mitotic DNA damage repair, but their roles within the context of meiotic recombination are less clear. In meiotic recombination, multiple repair pathways are used to repair meiotic DSBs, and current studies suggest that BLM may regulate the use of these pathways. Based on literature from Saccharomyces cerevisiae, Arabidopsis thaliana, Mus musculus, Drosophila melanogaster, and Caenorhabditis elegans, we present a unified model for a critical meiotic role of BLM and its orthologs...
September 2017: BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology
M Herbette, M G Mercier, F Michal, D Cluet, C Burny, G Yvert, V J Robert, F Palladino
Maintaining the integrity of genetic information across generations is essential for both cell survival and reproduction, and requires the timely repair of DNA damage. Histone-modifying enzymes play a central role in the DNA repair process through the deposition and removal of post-translational modifications on the histone tails. Specific histone modification act in the DNA repair process through the recruitment of proteins and complexes with specific enzymatic activities, or by altering the chromatin state at the site of DNA lesions...
September 2017: DNA Repair
Hilary K DeBardeleben, Lindsey E Lopes, Mark P Nessel, David M Raizen
Stress-induced sleep (SIS) in Caenorhabditis elegans is important for restoration of cellular homeostasis and is a useful model to study the function and regulation of sleep. SIS is triggered when epidermal growth factor (EGF) activates the ALA neuron, which then releases neuropeptides to promote sleep. To further understand this behavior, we established a new model of SIS using irradiation by ultraviolet C (UVC) light. While UVC irradiation requires ALA signaling and leads to a sleep state similar to that induced by heat and other stressors, it does not induce the proteostatic stress seen with heat exposure...
October 2017: Genetics
Raymund Bueno, Jessica C Mar
Synthetic lethal interactions (SLIs) are robust mechanisms that provide cells with the ability to remain viable despite having mutations in genes critical to the DNA damage response, a core cellular process. Studies in model organisms such as S. cerevisiae showed that thousands of genes important in maintaining DNA integrity cooperated in a SLI network. Two genes participate in a SLI when a mutation in one gene has no effect on the cell, but mutations in both interacting genes are lethal. Furthermore in C. elegans, a mutation in a critical gene that is important for development induced a change in expression variability in the synthetic lethal interactor...
July 25, 2017: Methods: a Companion to Methods in Enzymology
Joseph A Dawson, Caitlin Methven-Kelley, Gregory M Davis
Exchange of genetic information during meiosis occurs in all sexually reproducing species to produce haploid gametes from diploid cells. This process involves tight coordination of a meiotic specific cohesin complex, the synaptonemal complex, and DNA damage repair mechanisms. In this study, we describe a putative myosin heavy chain protein orthologous to human myosin 1, F28D1.2, which we named Abnormal Transition Zone (atz-1). Deletion of atz-1 results in embryonic lethality and a depleted transition zone, accompanied by reduced expression of the meiotic cohesin protein, REC-8...
July 11, 2017: Cell Biology International
Víctor González-Huici, Bin Wang, Anton Gartner
Ionizing radiation (IR) is commonly used in cancer therapy and is a main source of DNA double-strand breaks (DSBs), one of the most toxic forms of DNA damage. We have used Caenorhabditis elegans as an invertebrate model to identify novel factors required for repair of DNA damage inflicted by IR. We have performed an unbiased genetic screen, finding that smg-1 mutations confer strong hyper-sensitivity to IR. SMG-1 is a phosphoinositide-3 kinase (PI3K) involved in mediating nonsense-mediated mRNA decay (NMD) of transcripts containing premature stop codons and related to the ATM and ATR kinases which are at the apex of DNA damage signaling pathways...
August 2017: Genetics
Andrew R Mendelsohn, James W Larrick
NAD+ levels decline with age in diverse animals from Caenorhabditis elegans to mice. Raising NAD+ levels by dietary supplementation with NAD+ precursors, nicotinamide riboside (NR) or nicotinamide mononucleotide (NMN), improves mitochondrial function and muscle and neural and melanocyte stem cell function in mice, as well as increases murine life span. Decreased NAD+ levels with age reduce SIRT1 function and reduce the mitochondrial unfolded protein response, which can be overcome by NR supplementation. Decreased NAD+ levels cause NAD+-binding protein DBC1 to form a complex with PARP1, inhibiting poly(adenosine diphosphate-ribose) polymerase (PARP) catalytic activity...
June 2017: Rejuvenation Research
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