keyword
MENU ▼
Read by QxMD icon Read
search

Elegans dna damage

keyword
https://www.readbyqxmd.com/read/28506208/a-strategy-to-apply-quantitative-epistasis-analysis-on-developmental-traits
#1
Marta K Labocha, Wang Yuan, Boanerges Aleman-Meza, Weiwei Zhong
BACKGROUND: Genetic interactions are keys to understand complex traits and evolution. Epistasis analysis is an effective method to map genetic interactions. Large-scale quantitative epistasis analysis has been well established for single cells. However, there is a substantial lack of such studies in multicellular organisms and their complex phenotypes such as development. Here we present a method to extend quantitative epistasis analysis to developmental traits. METHODS: In the nematode Caenorhabditis elegans, we applied RNA interference on mutants to inactivate two genes, used an imaging system to quantitatively measure phenotypes, and developed a set of statistical methods to extract genetic interactions from phenotypic measurement...
May 15, 2017: BMC Genetics
https://www.readbyqxmd.com/read/28472769/spatial-function-of-the-oxidative-dna-damage-response-in-radiation-induced-bystander-effects-in-intra-and-inter-system-of-caenorhabditis-elegans
#2
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...
April 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/28472716/combined-loss-of-three-dna-damage-response-pathways-renders-c-elegans-intolerant-to-light
#3
Ivo van Bostelen, Marcel Tijsterman
Infliction of DNA damage initiates a complex cellular reaction - the DNA damage response - that involves both signaling and DNA repair networks with many redundancies and parallel pathways. Here, we reveal the three strategies that the simple multicellular eukaryote, C. elegans, uses to deal with DNA damage induced by light. Separately inactivating repair or replicative bypass of photo-lesions results in cellular hypersensitivity towards UV-light, but impeding repair of replication associated DNA breaks does not...
April 14, 2017: DNA Repair
https://www.readbyqxmd.com/read/28463453/a-simple-answer-to-complex-questions-c-elegans-as-an-experimental-model-for-examining-the-dna-damage-response-and-disease-genes
#4
Matthias Rieckher, Arturo Bujarrabal, Markus A Doll, Najmeh Soltanmohammadi, Björn Schumacher
The genetic information is constantly challenged by genotoxic attacks. DNA repair mechanisms evolved early in evolution and recognize and remove the various lesions. A complex network of DNA damage responses (DDR) orchestrates a variety of physiological adaptations to the presence of genome instability. Erroneous repair or malfunctioning of the DDR causes cancer development and the accumulation of DNA lesions drives the aging process. For understanding the complex DNA repair and DDR mechanisms it is pivotal to employ simple metazoan as model systems...
May 2, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28431244/bacterial-metabolism-affects-the-c-%C3%A2-elegans-response-to-cancer-chemotherapeutics
#5
Aurian P García-González, Ashlyn D Ritter, Shaleen Shrestha, Erik C Andersen, L Safak Yilmaz, Albertha J M Walhout
The human microbiota greatly affects physiology and disease; however, the contribution of bacteria to the response to chemotherapeutic drugs remains poorly understood. Caenorhabditis elegans and its bacterial diet provide a powerful system to study host-bacteria interactions. Here, we use this system to study how bacteria affect the C. elegans response to chemotherapeutics. We find that different bacterial species can increase the response to one drug yet decrease the effect of another. We perform genetic screens in two bacterial species using three chemotherapeutic drugs: 5-fluorouracil (5-FU), 5-fluoro-2'-deoxyuridine (FUDR), and camptothecin (CPT)...
April 20, 2017: Cell
https://www.readbyqxmd.com/read/28369609/4-bromodiphenyl-ether-bde-3-induces-germ-cell-apoptosis-by-induction-of-ros-and-dna-damage-in-caenorhabditis-elegans
#6
Xinyue You, Jing Xi, Yiyi Cao, Jinfu Zhang, Yang Luan
Polybrominated diphenyl ethers (PBDEs) may affect male reproductive function; however, the underlying mechanism is still uncertain. By using Caenorhabditis elegans (C. elegans), a commonly used model to study basic biological processes in apoptosis, we investigated the toxic effects of 4-bromodiphenyl ether (BDE-3), the most fundamental mono-BDE generated from degradation of PBDEs in the environment. We found that BDE-3 treated worms exhibited decreased life spans, impaired fecundity and delayed egg laying...
March 27, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28315685/abcb10-depletion-reduces-unfolded-protein-response-in-mitochondria
#7
Masato Yano
Mitochondria have many functions, including ATP generation. The electron transport chain (ETC) and the coupled ATP synthase generate ATP by consuming oxygen. Reactive oxygen species (ROS) are also produced by ETC, and ROS damage deoxyribonucleic acids, membrane lipids and proteins. Recent analysis indicate that mitochondrial unfolded protein response (UPR(mt)), which enhances expression of mitochondrial chaperones and proteases to remove damaged proteins, is activated when damaged proteins accumulate in the mitochondria...
March 16, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28299394/caenorhabditis-elegans-as-a-powerful-alternative-model-organism-to-promote-research-in-genetic-toxicology-and-biomedicine
#8
REVIEW
Sebastian Honnen
In view of increased life expectancy the risk for disturbed integrity of genetic information increases. This inevitably holds the implication for higher incidence of age-related diseases leading to considerable cost increase in health care systems. To develop preventive strategies it is crucial to evaluate external and internal noxae as possible threats to our DNA. Especially the interplay of DNA damage response (DDR) and DNA repair (DR) mechanisms needs further deciphering. Moreover, there is a distinct need for alternative in vivo test systems for basic research and also risk assessment in toxicology...
March 15, 2017: Archives of Toxicology
https://www.readbyqxmd.com/read/28242054/effects-of-methyl-and-inorganic-mercury-exposure-on-genome-homeostasis-and-mitochondrial-function-in-caenorhabditis-elegans
#9
Lauren H Wyatt, Anthony L Luz, Xiou Cao, Laura L Maurer, Ashley M Blawas, Alejandro Aballay, William K Y Pan, Joel N Meyer
Mercury toxicity mechanisms have the potential to induce DNA damage and disrupt cellular processes, like mitochondrial function. Proper mitochondrial function is important for cellular bioenergetics and immune signaling and function. Reported impacts of mercury on the nuclear genome (nDNA) are conflicting and inconclusive, and mitochondrial DNA (mtDNA) impacts are relatively unknown. In this study, we assessed genotoxic (mtDNA and nDNA), metabolic, and innate immune impacts of inorganic and organic mercury exposure in Caenorhabditis elegans...
April 2017: DNA Repair
https://www.readbyqxmd.com/read/28237114/monitoring-autophagic-responses-in-caenorhabditis-elegans
#10
M E Papandreou, N Tavernarakis
Autophagy, from the Greek auto (self) and phagy (eating), is a self-degradative process critical for eukaryotic cell homeostasis. Its rapidly responsive, highly dynamic nature renders this process essential for adapting to and offsetting acute/harsh conditions such as starvation, organelle dysfunction, and deoxyribonucleic acid (DNA) damage. Autophagy involves an intricate network of interacting factors with multiple levels of control. Importantly, dysregulation of autophagy has been linked to numerous debilitating pathologies, including cancer and neurodegenerative conditions in humans...
2017: Methods in Enzymology
https://www.readbyqxmd.com/read/28230788/the-adverse-effects-of-triptolide-on-the-reproductive-system-of-caenorhabditis-elegans-oogenesis-impairment-and-decreased-oocyte-quality
#11
Qinli Ruan, Yun Xu, Rui Xu, Jiaying Wang, Yongqing Hua, Meng Wang, Jinao Duan
Previous studies have revealed that Triptolide damages female reproductive capacity, but the mechanism is unclear. In this study, we used Caenorhabditis elegans to investigate the effects of Triptolide on the germline and explore its possible mechanisms. Our data show that exposure for 4 h to 50 and 100 mg/L Triptolide reduced C. elegans fertility, led to depletion and inactivation of spermatids with the changes in the expression levels of related genes, and increased the number of unfertilized oocytes through damaging chromosomes and DNA damage repair mechanisms...
February 21, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28223526/hypermutation-signature-reveals-a-slippage-and-realignment-model-of-translesion-synthesis-by-rev3-polymerase-in-cisplatin-treated-yeast
#12
Romulo Segovia, Yaoqing Shen, Scott A Lujan, Steven J M Jones, Peter C Stirling
Gene-gene or gene-drug interactions are typically quantified using fitness as a readout because the data are continuous and easily measured in high throughput. However, to what extent fitness captures the range of other phenotypes that show synergistic effects is usually unknown. Using Saccharomyces cerevisiae and focusing on a matrix of DNA repair mutants and genotoxic drugs, we quantify 76 gene-drug interactions based on both mutation rate and fitness and find that these parameters are not connected. Independent of fitness defects, we identified six cases of synthetic hypermutation, where the combined effect of the drug and mutant on mutation rate was greater than predicted...
March 7, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28088539/the-dna-damage-response-of-c-elegans-affected-by-gravity-sensing-and-radiosensitivity-during-the-shenzhou-8-spaceflight
#13
Ying Gao, Dan Xu, Lei Zhao, Yeqing Sun
Space radiation and microgravity are recognized as primary and inevitable risk factors for humans traveling in space, but the reports regarding their synergistic effects remain inconclusive and vary across studies due to differences in the environmental conditions and intrinsic biological sensitivity. Thus, we studied the synergistic effects on transcriptional changes in the global genome and DNA damage response (DDR) by using dys-1 mutant and ced-1 mutant of C. elegans, which respectively presented microgravity-insensitivity and radiosensitivity when exposure to spaceflight condition (SF) and space radiation (SR)...
January 2017: Mutation Research
https://www.readbyqxmd.com/read/28041875/snev-hprp19-hpso4-regulates-adipogenesis-of-human-adipose-stromal-cells
#14
Abdulhameed Khan, Hanna Dellago, Lucia Terlecki-Zaniewicz, Michael Karbiener, Sylvia Weilner, Florian Hildner, Viktoria Steininger, Christian Gabriel, Christoph Mück, Pidder Jansen-Dürr, Ara Hacobian, Marcel Scheideler, Regina Grillari-Voglauer, Markus Schosserer, Johannes Grillari
Aging is accompanied by loss of subcutaneous adipose tissue. This may be due to reduced differentiation capacity or deficiency in DNA damage repair (DDR) factors. Here we investigated the role of SNEV(hPrp19/hPso4), which was implicated in DDR and senescence evasion, in adipogenic differentiation of human adipose stromal cells (hASCs). We showed that SNEV is induced during adipogenesis and localized both in the nucleus and in the cytoplasm. Knockdown of SNEV perturbed adipogenic differentiation and led to accumulation of DNA damage in hASCs upon oxidative stress...
January 10, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28035971/aflatoxin-b%C3%A2-induced-developmental-and-dna-damage-in-caenorhabditis-elegans
#15
Wei-Hong Feng, Kathy S Xue, Lili Tang, Phillip L Williams, Jia-Sheng Wang
Aflatoxin B₁ (AFB₁) is a ubiquitous mycotoxin produced by toxicogenic Aspergillus species. AFB₁ has been reported to cause serious adverse health effects, such as cancers and abnormal development and reproduction, in animals and humans. AFB₁ is also a potent genotoxic mutagen that causes DNA damage in vitro and in vivo. However, the link between DNA damage and abnormal development and reproduction is unclear. To address this issue, we examined the DNA damage, germline apoptosis, growth, and reproductive toxicity following exposure to AFB₁, using Caenorhabditis elegans as a study model...
December 26, 2016: Toxins
https://www.readbyqxmd.com/read/27956467/linc-complexes-promote-homologous-recombination-in-part-through-inhibition-of-nonhomologous-end-joining
#16
Katherine S Lawrence, Erin C Tapley, Victor E Cruz, Qianyan Li, Kayla Aung, Kevin C Hart, Thomas U Schwartz, Daniel A Starr, JoAnne Engebrecht
The Caenorhabditis elegans SUN domain protein, UNC-84, functions in nuclear migration and anchorage in the soma. We discovered a novel role for UNC-84 in DNA damage repair and meiotic recombination. Loss of UNC-84 leads to defects in the loading and disassembly of the recombinase RAD-51. Similar to mutations in Fanconi anemia (FA) genes, unc-84 mutants and human cells depleted of Sun-1 are sensitive to DNA cross-linking agents, and sensitivity is rescued by the inactivation of nonhomologous end joining (NHEJ)...
December 19, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27874324/interaction-between-radioadaptive-response-and-radiation-induced-bystander-effect-in-caenorhabditis-elegans-a-unique-role-of-the-dna-damage-checkpoint
#17
Huangqi Tang, Liangwen Chen, Lianyun Chen, Bin Chen, Ting Wang, Aifeng Yang, Furu Zhan, Lijun Wu, Po Bian
Although radioadaptive responses (RAR) and radiation-induced bystander effects (RIBE) are two important biological effects of low-dose radiation, there are currently only limited data that directly address their interaction, particularly in the context of whole organisms. In previous studies, we separately demonstrated RAR and RIBE using an in vivo system of C. elegans . In the current study, we further investigated their interaction in C. elegans , with the ratio of protruding vulva as the biological end point for RAR...
December 2016: Radiation Research
https://www.readbyqxmd.com/read/27831827/mitotic-entry-the-interplay-between-cdk1-plk1-and-bora
#18
Alfonso Parrilla, Luca Cirillo, Yann Thomas, Monica Gotta, Lionel Pintard, Anna Santamaria
Polo-like kinase 1 (Plk1) is an important mitotic kinase that is crucial for entry into mitosis after recovery from DNA damage-induced cell cycle arrest. Plk1 activation is promoted by the conserved protein Bora (SPAT-1 in C. elegans), which stimulates the phosphorylation of a conserved residue in the activation loop by the Aurora A kinase. In a recent article published in Cell Reports, we show that the master mitotic kinase Cdk1 contributes to Plk1 activation through SPAT-1/Bora phosphorylation. We identified 3 conserved Sp/Tp residues that are located in the N-terminal, most conserved part, of SPAT-1/Bora...
December 2016: Cell Cycle
https://www.readbyqxmd.com/read/27803194/quantification-of-in-vivo-progenitor-mutation-accrual-with-ultra-low-error-rate-and-minimal-input-dna-using-sip-hava-seq
#19
Pete H Taylor, Amanda Cinquin, Olivier Cinquin
Assaying in vivo accrual of DNA damage and DNA mutations by stem cells and pinpointing sources of damage and mutations would further our understanding of aging and carcinogenesis. Two main hurdles must be overcome. First, in vivo mutation rates are orders of magnitude lower than raw sequencing error rates. Second, stem cells are vastly outnumbered by differentiated cells, which have a higher mutation rate-quantification of stem cell DNA damage and DNA mutations is thus best performed from small, well-defined cell populations...
November 2016: Genome Research
https://www.readbyqxmd.com/read/27791127/cockayne-syndrome-group-a-and-b-proteins-converge-on-transcription-linked-resolution-of-non-b-dna
#20
Morten Scheibye-Knudsen, Anne Tseng, Martin Borch Jensen, Karsten Scheibye-Alsing, Evandro Fei Fang, Teruaki Iyama, Sanjay Kumar Bharti, Krisztina Marosi, Lynn Froetscher, Henok Kassahun, David Mark Eckley, Robert W Maul, Paul Bastian, Supriyo De, Soumita Ghosh, Hilde Nilsen, Ilya G Goldberg, Mark P Mattson, David M Wilson, Robert M Brosh, Myriam Gorospe, Vilhelm A Bohr
Cockayne syndrome is a neurodegenerative accelerated aging disorder caused by mutations in the CSA or CSB genes. Although the pathogenesis of Cockayne syndrome has remained elusive, recent work implicates mitochondrial dysfunction in the disease progression. Here, we present evidence that loss of CSA or CSB in a neuroblastoma cell line converges on mitochondrial dysfunction caused by defects in ribosomal DNA transcription and activation of the DNA damage sensor poly-ADP ribose polymerase 1 (PARP1). Indeed, inhibition of ribosomal DNA transcription leads to mitochondrial dysfunction in a number of cell lines...
November 1, 2016: Proceedings of the National Academy of Sciences of the United States of America
keyword
keyword
59954
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"