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https://www.readbyqxmd.com/read/28087659/plant-parasitic-nematodes-towards-understanding-molecular-players-in-stress-responses
#1
REVIEW
François-Xavier Gillet, Caroline Bournaud, Jose Dijair Antonino de Souza Júnior, Maria Fatima Grossi-de-Sa
BACKGROUND: Plant-parasitic nematode interactions occur within a vast molecular plant immunity network. Following initial contact with the host plant roots, plant-parasitic nematodes (PPNs) activate basal immune responses. Defence priming involves the release in the apoplast of toxic molecules derived from reactive species or secondary metabolism. In turn, PPNs must overcome the poisonous and stressful environment at the plant-nematode interface. The ability of PPNs to escape this first line of plant immunity is crucial and will determine its virulence...
January 13, 2017: Annals of Botany
https://www.readbyqxmd.com/read/28079896/impaired-embryonic-development-in-glucose-6-phosphate-dehydrogenase-deficient-caenorhabditis-elegans-due-to-abnormal-redox-homeostasis-induced-activation-of-calcium-independent-phospholipase-and-alteration-of-glycerophospholipid-metabolism
#2
Tzu-Ling Chen, Hung-Chi Yang, Cheng-Yu Hung, Meng-Hsin Ou, Yi-Yun Pan, Mei-Ling Cheng, Arnold Stern, Szecheng J Lo, Daniel Tsun-Yee Chiu
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly pervasive inherited disease in many parts of the world. The complete lack of G6PD activity in a mouse model causes embryonic lethality. The G6PD-deficient Caenorhabditis elegans model also shows embryonic death as indicated by a severe hatching defect. Although increased oxidative stress has been implicated in both cases as the underlying cause, the exact mechanism has not been clearly delineated. In this study with C. elegans, membrane-associated defects, including enhanced permeability, defective polarity and cytokinesis, were found in G6PD-deficient embryos...
January 12, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28076789/reduced-insulin-igf-1-signaling-restores-the-dynamic-properties-of-key-stress-granule-proteins-during-aging
#3
Marie C Lechler, Emily D Crawford, Nicole Groh, Katja Widmaier, Raimund Jung, Janine Kirstein, Jonathan C Trinidad, Alma L Burlingame, Della C David
Low-complexity "prion-like" domains in key RNA-binding proteins (RBPs) mediate the reversible assembly of RNA granules. Individual RBPs harboring these domains have been linked to specific neurodegenerative diseases. Although their aggregation in neurodegeneration has been extensively characterized, it remains unknown how the process of aging disturbs RBP dynamics. We show that a wide variety of RNA granule components, including stress granule proteins, become highly insoluble with age in C. elegans and that reduced insulin/insulin-like growth factor 1 (IGF-1) daf-2 receptor signaling efficiently prevents their aggregation...
January 10, 2017: Cell Reports
https://www.readbyqxmd.com/read/28067237/environmental-stresses-induce-transgenerationally-inheritable-survival-advantages-via-germline-to-soma-communication-in-caenorhabditis-elegans
#4
Saya Kishimoto, Masaharu Uno, Emiko Okabe, Masanori Nono, Eisuke Nishida
Hormesis is a biological phenomenon, whereby exposure to low levels of toxic agents or conditions increases organismal viability. It thus represents a beneficial aspect of adaptive responses to harmful environmental stimuli. Here we show that hormesis effects induced in the parental generation can be passed on to the descendants in Caenorhabditis elegans. Animals subjected to various stressors during developmental stages exhibit increased resistance to oxidative stress and proteotoxicity. The increased resistance is transmitted to the subsequent generations grown under unstressed conditions through epigenetic alterations...
January 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28049353/nicotine-affects-protein-complex-rearrangement-in-caenorhabditis-elegans-cells
#5
Robert Sobkowiak, Andrzej Zielezinski, Wojciech M Karlowski, Andrzej Lesicki
Nicotine may affect cell function by rearranging protein complexes. We aimed to determine nicotine-induced alterations of protein complexes in Caenorhabditis elegans (C. elegans) cells, thereby revealing links between nicotine exposure and protein complex modulation. We compared the proteomic alterations induced by low and high nicotine concentrations (0.01 mM and 1 mM) with the control (no nicotine) in vivo by using mass spectrometry (MS)-based techniques, specifically the cetyltrimethylammonium bromide (CTAB) discontinuous gel electrophoresis coupled with liquid chromatography (LC)-MS/MS and spectral counting...
January 3, 2017: Drug and Chemical Toxicology
https://www.readbyqxmd.com/read/28043053/the-decay-of-redox-stress-response-capacity-is-a-substantive-characteristic-of-aging-revising-the-redox-theory-of-aging
#6
Jiao Meng, Zhenyu Lv, Xinhua Qiao, Xiaopeng Li, Yazi Li, Yuying Zhang, Chang Chen
Aging is tightly associated with redox events. The free radical theory of aging indicates that redox imbalance may be an important factor in the aging process. Most studies about redox and aging focused on the static status of oxidative stress levels, there has been little research investigating differential responses to redox challenge during aging. In this study, we used Caenorhabditis elegans and human fibroblasts as models to compare differential responses to oxidative stress challenge in young and old individuals...
December 28, 2016: Redox Biology
https://www.readbyqxmd.com/read/28041875/snev-hprp19-hpso4-regulates-adipogenesis-of-human-adipose-stromal-cells
#7
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/28039083/2-3-dehydrosilybin-a-b-as-a-pro-longevity-and-anti-aggregation-compound
#8
Konstantina Filippopoulou, Nikoletta Papaevgeniou, Maria Lefaki, Anna Paraskevopoulou, David Biedermann, Vladimír Křen, Niki Chondrogianni
Aging is an unavoidable process characterized by gradual failure of homeostasis that constitutes a critical risk factor for several age-related disorders. It has been unveiled that manipulation of various key pathways may decelerate the aging progression and the triggering of age-related diseases. As a consequence, the identification of compounds, preferably natural-occurring, administered through diet, with lifespan-extending, anti-aggregation and anti-oxidation properties that in parallel exhibit negligible side-effects is the main goal in the battle against aging...
December 28, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28028818/a-mechanism-for-sickness-sleep-lessons-from-invertebrates
#9
Kristen C Davis, David M Raizen
During health, animal sleep is regulated by an internal clock and by the duration of prior wakefulness. During sickness, sleep is regulated by cytokines released from either peripheral cells or from cells within the nervous system. These cytokines regulate central nervous system neurons to induce sleep. Recent research in the invertebrates Caenorhabditis elegans and Drosophila melanogaster has led to new insights into the mechanism of sleep during sickness. Sickness is triggered by exposure to environments such as infection, heat, or ultraviolet light irradiation, all of which cause cellular stress...
December 28, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27989695/the-genetics-of-isoflurane-induced-developmental-neurotoxicity
#10
Hyo-Seok Na, Nicole L Brockway, Katherine R Gentry, Elyce Opheim, Margaret M Sedensky, Philip G Morgan
INTRODUCTION: Neurotoxicity induced by early developmental exposure to volatile anesthetics is a characteristic of organisms across a wide range of species, extending from the nematode C. elegans to mammals. Prevention of anesthetic-induced neurotoxicity (AIN) will rely upon an understanding of its underlying mechanisms. However, no forward genetic screens have been undertaken to identify the critical pathways affected in AIN.By characterizing such pathways, we may identify mechanisms to eliminate isoflurane induced AIN in mammals...
October 28, 2016: Neurotoxicology and Teratology
https://www.readbyqxmd.com/read/27986570/the-c-box-region-of-maf1-regulates-transcriptional-activity-and-protein-stability
#11
Ajay Pradhan, Amy M Hammerquist, Akshat Khanna, Sean P Curran
MAF1 is a conserved negative regulator of RNA polymerase (pol) III and intracellular lipid homeostasis across species. Here, we show that the MAF1 C-box region negatively regulates its activity. Mutations in Caenorhabditis elegans mafr-1 that truncate the C-box retain the ability to inhibit the transcription of RNA pol III targets, reduce lipid biogenesis, and lower reproductive output. In human cells, C-box deletion of MAF1 leads to increased MAF1 nuclear localization and enhanced repression of ACC1 and FASN, but with impaired repression of RNA pol III targets...
December 13, 2016: Journal of Molecular Biology
https://www.readbyqxmd.com/read/27982058/shengmai-formula-suppressed-over-activated-ras-mapk-pathway-in-c-elegans-by-opening-mitochondrial-permeability-transition-pore-via-regulating-cyclophilin-d
#12
Yan Liu, Dejuan Zhi, Menghui Li, Dongling Liu, Xin Wang, Zhengrong Wu, Zhanxin Zhang, Dongqing Fei, Yang Li, Hongmei Zhu, Qingjian Xie, Hui Yang, Hongyu Li
Since about 30% of all human cancers contain mutationally activated Ras, down regulating the over-activation of Ras/MAPK pathway represents a viable approach for treating cancers. Over-activation of Ras/MAPK pathway is accompanied by accumulation of reactive oxygen species (ROS). One approach for developing anti-cancer drugs is to target ROS production and their accumulation. To test this idea, we have employed C. elegans of let-60 (gf) mutant, which contain over-activated let-60 (the homolog of mammalian ras) and exhibit tumor-like symptom of multivulva phenotype, to determine whether anti-oxidants can affect their tumor-like phenotype...
December 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27979995/nucleosome-fragility-is-associated-with-future-transcriptional-response-to-developmental-cues-and-stress-in-c-elegans
#13
Tess E Jeffers, Jason D Lieb
Nucleosomes have structural and regulatory functions in all eukaryotic DNA-templated processes. The position of nucleosomes on DNA and the stability of the underlying histone-DNA interactions affect the access of regulatory proteins to DNA. Both stability and position are regulated through DNA sequence, histone post-translational modifications, histone variants, chromatin remodelers, and transcription factors. Here, we explored the functional implications of nucleosome properties on gene expression and development in Caenorhabditis elegans embryos...
January 2017: Genome Research
https://www.readbyqxmd.com/read/27974500/starvation-induced-stress-response-is-critically-impacted-by-ceramide-levels-in-caenorhabditis-elegans
#14
Mingxue Cui, Yi Wang, Jonathon Cavaleri, Taylor Kelson, Yudong Teng, Min Han
Our understanding of the cellular mechanisms by which animals regulate their response to starvation is limited despite the strong relevance of the problem to major human health issues. The L1 diapause of Caenorhabditis elegans, where first-stage larvae arrest in response to a food-less environment, is an excellent system to study this mechanism. We found through genetic manipulation and lipid analysis that ceramide biosynthesis, particularly those with longer fatty acid side chains, critically impacts animal survival during L1 diapause...
December 14, 2016: Genetics
https://www.readbyqxmd.com/read/27974198/proline-catabolism-modulates-innate-immunity-in-caenorhabditis-elegans
#15
Haiqing Tang, Shanshan Pang
Metabolic pathways are regulated to fuel or instruct the immune responses to pathogen threats. However, the regulatory roles for amino acid metabolism in innate immune responses remains poorly understood. Here, we report that mitochondrial proline catabolism modulates innate immunity in Caenorhabditis elegans. Modulation of proline catabolic enzymes affects host susceptibility to bacterial pathogen Pseudomonas aeruginosa. Mechanistically, proline catabolism governs reactive oxygen species (ROS) homeostasis and subsequent activation of SKN-1, a critical transcription factor regulating xenobiotic stress response and pathogen defense...
December 13, 2016: Cell Reports
https://www.readbyqxmd.com/read/27940089/the-ancient-cytokine-il-17d-is-regulated-by-nrf2-and-mediates-tumor-and-virus-surveillance
#16
Ruth Seelige, Allen Washington, Jack D Bui
Early stage immune responses can dictate the severity and outcome of inflammatory processes such as tumor growth and viral infection. Cytokines such as the interleukin 17 (IL-17) family and cellular stress defense (e.g., anti-oxidant) pathways have evolved early and regulate disease surveillance in vertebrates and invertebrates as far back as Caenorhabditis elegans. Our group has recently found a new role for nuclear factor erythroid-derived 2-like 2 (Nrf2) in regulating early anti-cancer immune responses by inducing IL-17D and recruiting natural killer (NK) cells...
December 8, 2016: Cytokine
https://www.readbyqxmd.com/read/27927209/coordinated-inhibition-of-c-ebp-by-tribbles-in-multiple-tissues-is-essential-for-caenorhabditis-elegans-development
#17
Kyung Won Kim, Nishant Thakur, Christopher A Piggott, Shizue Omi, Jolanta Polanowska, Yishi Jin, Nathalie Pujol
BACKGROUND: Tribbles proteins are conserved pseudokinases that function to control kinase signalling and transcription in diverse biological processes. Abnormal function in human Tribbles has been implicated in a number of diseases including leukaemia, metabolic syndromes and cardiovascular diseases. Caenorhabditis elegans Tribbles NIPI-3 was previously shown to activate host defense upon infection by promoting the conserved PMK-1/p38 mitogen-activated protein kinase (MAPK) signalling pathway...
December 7, 2016: BMC Biology
https://www.readbyqxmd.com/read/27922032/chemically-induced-oxidative-stress-affects-ash-neuronal-function-and-behavior-in-c-elegans
#18
Eleni Gourgou, Nikos Chronis
Oxidative stress (OS) impact on a single neuron's function in vivo remains obscure. Using C. elegans as a model organism, we report the effect of paraquat (PQ)-induced OS on wild type worms on the function of the ASH polymodal neuron. By calcium (Ca(2+)) imaging, we quantified ASH activation upon stimulus delivery. PQ-treated worms displayed higher maximum depolarization (peak of the Ca(2+) transients) compared to untreated animals. PQ had a similar effect on the ASH neuron response time (rising slope of the Ca(2+) transients), except in very young worms...
December 6, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27911941/copper-oxide-nanoparticles-impact-several-toxicological-endpoints-and-cause-neurodegeneration-in-caenorhabditis-elegans
#19
Michael J Mashock, Tyler Zanon, Anthony D Kappell, Lisa N Petrella, Erik C Andersen, Krassimira R Hristova
Engineered nanoparticles are becoming increasingly incorporated into technology and consumer products. In 2014, over 300 tons of copper oxide nanoparticles were manufactured in the United States. The increased production of nanoparticles raises concerns regarding the potential introduction into the environment or human exposure. Copper oxide nanoparticles commonly release copper ions into solutions, which contribute to their toxicity. We quantified the inhibitory effects of both copper oxide nanoparticles and copper sulfate on C...
2016: PloS One
https://www.readbyqxmd.com/read/27905558/microrna-mir-34-provides-robustness-to-environmental-stress-response-via-the-daf-16-network-in-c-elegans
#20
Meltem Isik, T Keith Blackwell, Eugene Berezikov
Diverse stresses and aging alter expression levels of microRNAs, suggesting a role for these posttranscriptional regulators of gene expression in stress modulation and longevity. Earlier studies demonstrated a central role for the miR-34 family in promoting cell cycle arrest and cell death following stress in human cells. However, the biological significance of this response was unclear. Here we show that in C. elegans mir-34 upregulation is necessary for developmental arrest, correct morphogenesis, and adaptation to a lower metabolic state to protect animals against stress-related damage...
December 1, 2016: Scientific Reports
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