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C elegans aging

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https://www.readbyqxmd.com/read/29123644/rnai-targeting-caenorhabditis-elegans-%C3%AE-arrestins-marginally-affects-lifespan
#1
Sangsoon Park, Yoonji Jung, Seon Woo A An, Heehwa G Son, Wooseon Hwang, Dongyeop Lee, Murat Artan, Hae-Eun H Park, Dae-Eun Jeong, Yujin Lee, Seung-Jae V Lee
Background: α-arrestins are a family of proteins that are implicated in multiple biological processes, including metabolism and receptor desensitization. Methods: Here, we sought to examine the roles of α-arrestins in the longevity of Caenorhabditis elegans through an RNA interference screen. Results: We found that knocking down each of 24 out of total 29 C. elegans α-arrestins had small or no effects on lifespan. Thus, individual C. elegans α-arrestins may have minor effects on longevity. Conclusions: This study will provide useful information for future research on the functional role of α-arrestins in aging and longevity...
2017: F1000Research
https://www.readbyqxmd.com/read/29120414/genetic-variation-in-glia-neuron-signalling-modulates-ageing-rate
#2
Jiang-An Yin, Ge Gao, Xi-Juan Liu, Zi-Qian Hao, Kai Li, Xin-Lei Kang, Hong Li, Yuan-Hong Shan, Wen-Li Hu, Hai-Peng Li, Shi-Qing Cai
The rate of behavioural decline in the ageing population is remarkably variable among individuals. Despite the considerable interest in studying natural variation in ageing rate to identify factors that control healthy ageing, no such factor has yet been found. Here we report a genetic basis for variation in ageing rates in Caenorhabditis elegans. We find that C. elegans isolates show diverse lifespan and age-related declines in virility, pharyngeal pumping, and locomotion. DNA polymorphisms in a novel peptide-coding gene, named regulatory-gene-for-behavioural-ageing-1 (rgba-1), and the neuropeptide receptor gene npr-28 influence the rate of age-related decline of worm mating behaviour; these two genes might have been subjected to recent selective sweeps...
November 8, 2017: Nature
https://www.readbyqxmd.com/read/29114996/impaired-p53-cep-1-is-associated-with-lifespan-extension-through-an-age-related-imbalance-in-the-energy-metabolism-of-c-%C3%A2-elegans
#3
Sumino Yanase, Hitoshi Suda, Kayo Yasuda, Naoaki Ishii
In the nematode Caenorhabditis elegans, the mammalian tumor suppressor p53 ortholog CEP-1 mediates the stress response, activates germ line apoptosis and regulates meiotic chromosome segregation. A reduction in its expression, which frequently occurs in mammalian cancer cells, extends lifespan and induces an adaptive response in C. elegans. However, these effects do not involve an increase in oxidative stress resistance. Here, we showed that intermittent exposure to hyperoxia, which induces oxidative stress resistance and lowers the production of ROS derived from mitochondrial respiration in C...
November 8, 2017: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/29114017/a-microrna-feedback-loop-regulates-global-microrna-abundance-during-aging
#4
Sachi Inukai, Zachary Pincus, Alexandre de Lencastre, Frank J Slack
Expression levels of many microRNAs (miRNAs) change during aging, notably declining globally in a number of organisms and tissues across taxa. However, little is known about the mechanisms or the biological relevance for this change. We investigated the network of genes that controls miRNA transcription and processing during C. elegans aging. We found that miRNA biogenesis genes are highly networked with transcription factors and aging-associated miRNAs. In particular, miR-71, known to influence lifespan and itself upregulated during aging, represses alg-1/Argonaute expression post-transcriptionally during aging...
November 7, 2017: RNA
https://www.readbyqxmd.com/read/29107506/dietary-restriction-and-ampk-increase-lifespan-via-mitochondrial-network-and-peroxisome-remodeling
#5
Heather J Weir, Pallas Yao, Frank K Huynh, Caroline C Escoubas, Renata L Goncalves, Kristopher Burkewitz, Raymond Laboy, Matthew D Hirschey, William B Mair
Mitochondrial network remodeling between fused and fragmented states facilitates mitophagy, interaction with other organelles, and metabolic flexibility. Aging is associated with a loss of mitochondrial network homeostasis, but cellular processes causally linking these changes to organismal senescence remain unclear. Here, we show that AMP-activated protein kinase (AMPK) and dietary restriction (DR) promote longevity in C. elegans via maintaining mitochondrial network homeostasis and functional coordination with peroxisomes to increase fatty acid oxidation (FAO)...
October 23, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/29103937/an-intracellular-pathogen-response-pathway-promotes-proteostasis-in-c-%C3%A2-elegans
#6
Kirthi C Reddy, Tal Dror, Jessica N Sowa, Johan Panek, Kevin Chen, Efrem S Lim, David Wang, Emily R Troemel
Maintenance of protein homeostasis, or proteostasis, is crucial for organismal health. Disruption of proteostasis can lead to the accumulation of protein aggregates, which are associated with aging and many human diseases such as Alzheimer's disease [1-3]. Through analysis of the C. elegans host response to intracellular infection, we describe here a novel response pathway that enhances proteostasis capacity and appears to act in parallel to well-studied proteostasis pathways. These findings are based on analysis of the transcriptional response to infection by the intracellular pathogen Nematocida parisii [4]...
October 30, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/29097398/cell-biology-of-the-mitochondrion
#7
Alexander M van der Bliek, Margaret M Sedensky, Phil G Morgan
Mitochondria are best known for harboring pathways involved in ATP synthesis through the tricarboxylic acid cycle and oxidative phosphorylation. Major advances in understanding these roles were made with Caenorhabditiselegans mutants affecting key components of the metabolic pathways. These mutants have not only helped elucidate some of the intricacies of metabolism pathways, but they have also served as jumping off points for pharmacology, toxicology, and aging studies. The field of mitochondria research has also undergone a renaissance, with the increased appreciation of the role of mitochondria in cell processes other than energy production...
November 2017: Genetics
https://www.readbyqxmd.com/read/29081084/mitochondrial-uncoupling-attenuates-age-dependent-neurodegeneration-in-c-elegans
#8
Injeong Cho, Hyun-Ok Song, Jeong Hoon Cho
The uncoupling protein 4 (ucp-4) gene is involved in agedependent neurodegeneration in C. elegans. Therefore, we aimed to investigate the mechanism underlying the association between mitochondrial uncoupling and neurodegeneration by examining the effects of uncoupling agents and ucp-4 overexpression in C. elegans. Treatment with either DNP or CCCP improved neuronal defects in wild type during aging.Uncoupling agents also restored neuronal phenotypes of ucp-4 mutants to those exhibited by wild type, while ucp-4 overexpression attenuated the severity of age-dependent neurodegeneration...
October 27, 2017: Molecules and Cells
https://www.readbyqxmd.com/read/29069955/shatavarin-iv-elicits-lifespan-extension-and-alleviates-parkinsonism-in-caenorhabditis-elegans
#9
Shachi Shuchi Smita, Shreesh Raj Sammi, Tulsankar S Laxman, Rabi S Bhatta, Rakesh Pandey
Shatavarin IV (SIV), a steroidal saponin is a major bioactive phytomolecule present in roots of Asparagus racemosus (Liliaceae) known for its anticancer activity. Age associated neurodegenerative Parkinson's disease (PD) is characterized by alpha-synuclein aggregation in dopaminergic neuron resulting in neurodegeneration. The invention of bioactive molecules that delay aging and age associated disorders endorses development of natural phytomolecule as a therapeutic agent for curing age related diseases. Therefore, present study for the first time explores the potential of SIV against aging and Parkinsonism utilizing Caenorhabditis elegans model system...
October 25, 2017: Free Radical Research
https://www.readbyqxmd.com/read/29053679/measuring-the-effect-of-chemicals-on-the-growth-and-reproduction-of-caenorhabditis-elegans
#10
So Young Lee, Kyungsu Kang
Toxicological evaluation is crucial for understanding the effects of chemicals on living organisms in basic and applied biological science fields. A non-mammalian soil round worm, Caenorhabditis elegans, is a valuable model organism for toxicology studies due to its convenience and lack of animal ethics issues compared with mammalian animal systems. In this protocol, a detailed procedure of toxicological evaluation of chemicals in C. elegans is described. A clinical anticancer drug, etoposide, which targets human topoisomerase II and inhibits DNA replication of human cancer cells, was selected as a model testing chemical...
October 5, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29049853/nutrient-driven-o-glcnac-in-proteostasis-and-neurodegeneration
#11
REVIEW
Ilhan Akan, Stephanie Olivier-Van Stichelen, Michelle R Bond, John A Hanover
Proteostasis is essential in the mammalian brain where post-mitotic cells must function for decades to maintain synaptic contacts and memory. The brain is dependent on glucose and other metabolites for proper function and is spared from metabolic deficits even during starvation. In this review, we outline how the nutrient sensitive nucleocytoplasmic posttranslational modification O-linked N-acetylglucosamine (O-GlcNAc) regulates protein homeostasis. The O-GlcNAc modification is highly abundant in the mammalian brain, and has been linked to proteopathies, including neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's...
October 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29048250/inhibition-of-abeta-proteotoxicity-by-paeoniflorin-in-i-caenorhabditis-elegans-i-through-regulation-of-oxidative-and-heat-shock-stress-responses
#12
Liping Ai, Fan Yang, Jie Song, Yan Chen, Lingyun Xiao, Qiangqiang Wang, Liangyi Wang, Haifeng Li, Tao Lei, Zebo Huang
Alzheimer's disease (AD) is a common form of dementia and amyloid-β peptide (Aβ) aggregation is considered to be one of its main causes. Paeoniflorin has been previously shown to attenuate cognitive damage inflicted by exogenous Aβ protein. Using transgenic <i>Caenorhabditis elegans</i> models expressing human Aβ1-42, we demonstrate here that paeoniflorin can delay progressive paralysis caused by endogenous Aβ expression and reduce the amount of toxic Aβ oligomers in vivo although it has no effect on Aβ aggregation <i>in vitro</i>...
October 19, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/29036691/nuclear-localized-c9orf72-associated-arginine-containing-dipeptides-exhibit-age-dependent-toxicity-in-c-elegans
#13
Paige Rudich, Carley Snoznik, Simon C Watkins, John Monaghan, Udai Bhan Pandey, Todd Lamitina
A hexanucleotide repeat expansion mutation in the C9orf72 gene represents a prevalent genetic cause of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Non-canonical translation of this repeat gives rise to several distinct dipeptide protein species that could play pathological roles in disease. Here, we show in the model system C. elegans that expression of the arginine-containing dipeptides, but not alanine-containing dipeptides, produces toxic phenotypes in multiple cellular contexts, including motor neurons...
September 27, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/29031405/life-span-resolved-nanotoxicology-enables-identification-of-age-associated-neuromuscular-vulnerabilities-in-the-nematode-caenorhabditis-elegans
#14
Annette Piechulek, Anna von Mikecz
At present, the majority of investigations concerning nanotoxicology in the nematode C. elegans address short-term effects. While this approach allows for the identification of uptake pathways, exposition and acute toxicity, nanoparticle-organism interactions that manifest later in the adult life of C. elegans are missed. Here we show that a microhabitat composed of liquid S-medium and live bacteria in microtiter wells prolongs C. elegans longevity and is optimally suited to monitor chronic eNP-effects over the entire life span (about 34 days) of the nematode...
October 11, 2017: Environmental Pollution
https://www.readbyqxmd.com/read/29030550/a-conserved-klf-autophagy-pathway-modulates-nematode-lifespan-and-mammalian-age-associated-vascular-dysfunction
#15
Paishiun N Hsieh, Guangjin Zhou, Yiyuan Yuan, Rongli Zhang, Domenick A Prosdocimo, Panjamaporn Sangwung, Anna H Borton, Evgenii Boriushkin, Anne Hamik, Hisashi Fujioka, Ciaran E Fealy, John P Kirwan, Maureen Peters, Yuan Lu, Xudong Liao, Diana Ramírez-Bergeron, Zhaoyang Feng, Mukesh K Jain
Loss of protein and organelle quality control secondary to reduced autophagy is a hallmark of aging. However, the physiologic and molecular regulation of autophagy in long-lived organisms remains incompletely understood. Here we show that the Kruppel-like family of transcription factors are important regulators of autophagy and healthspan in C. elegans, and also modulate mammalian vascular age-associated phenotypes. Kruppel-like family of transcription factor deficiency attenuates autophagy and lifespan extension across mechanistically distinct longevity nematode models...
October 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/29030433/dysregulation-of-the-mitochondrial-unfolded-protein-response-induces-non-apoptotic-dopaminergic-neurodegeneration-in-c-elegans-models-of-parkinson-s-disease
#16
Bryan A Martinez, Daniel A Petersen, Anthony L Gaeta, Samuel P Stanley, Guy A Caldwell, Kim A Caldwell
Due to environmental insult or innate genetic deficiency, protein folding environments of the mitochondrial matrix are prone to dysregulation, prompting the activation of a specific organellar stress-response mechanism, the mitochondrial unfolded protein response (UPR(MT)). In Caenorhabditis elegans, mitochondrial damage leads to nuclear translocation of the ATFS-1 transcription factor to activate the UPR(MT) After short-term acute stress has been mitigated, the UPR(MT) is eventually suppressed to restore homeostasis to C...
November 15, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29027899/metformin-extends-c-elegans-lifespan-through-lysosomal-pathway
#17
Jie Chen, Yuhui Ou, Yi Li, Shumei Hu, Li-Wa Shao, Ying Liu
Metformin, a widely used first-line drug for treatment of type 2 diabetes (T2D), has been shown to extend lifespan and delay the onset of age-related diseases. However, its primary locus of action remains unclear. Using a pure in vitro reconstitution system, we demonstrate that metformin acts through the v-ATPase-Ragulator lysosomal pathway to coordinate mTORC1 and AMPK, two hubs governing metabolic programs. We further show in Caenorhabditis elegans that both v-ATPase-mediated TORC1 inhibition and v-ATPase-AXIN/LKB1-mediated AMPK activation contribute to the lifespan extension effect of metformin...
October 13, 2017: ELife
https://www.readbyqxmd.com/read/29022701/genetic-and-pharmacological-discovery-for-alzheimer-s-disease-using-caenorhabditis-elegans
#18
Edward F Griffin, Kim A Caldwell, Guy A Caldwell
The societal burden presented by Alzheimer's disease warrants both innovative and expedient means by which its underlying molecular causes can be both identified and mechanistically exploited to discern novel therapeutic targets and strategies. The conserved characteristics, defined neuroanatomy, and advanced technological application of Caenorhabditis elegans render this metazoan an unmatched tool for probing neurotoxic factors. In addition, its short lifespan and importance in the field of aging make it an ideal organism for modeling age-related neurodegenerative disease...
October 25, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/28986305/high-throughput-biosorter-quantification-of-relative-mitochondrial-content-and-membrane-potential-in-living-caenorhabditis-elegans
#19
Young Joon Kwon, Sujay Guha, Florin Tuluc, Marni J Falk
Mitochondrial respiratory chain disease is caused by a wide range of individually rare genetic disorders that impair cellular energy metabolism. While fluorescence microscopy analysis of nematodes fed MitoTracker Green (MTG) and tetramethylrhodamine ethyl ester (TMRE) can reliably quantify relative mitochondrial density and membrane potential, respectively, in C. elegans, it is a tedious process with limitations in the number and age of animals that can be studied. A novel, large particle, flow cytometry-based method reported here accelerates and automates the relative quantitation of mitochondrial physiology in nematode populations...
October 3, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28983319/loss-of-sphingosine-kinase-alters-life-history-traits-and-locomotor-function-in-caenorhabditis-elegans
#20
Jason P Chan, Jaylene Brown, Brandon Hark, Abby Nolan, Dustin Servello, Hannah Hrobuchak, Trisha A Staab
Sphingolipid metabolism is important to balance the abundance of bioactive lipid molecules involved in cell signaling, neuronal function, and survival. Specifically, the sphingolipid sphingosine mediates cell death signaling, whereas its phosphorylated form, sphingosine-1-phosphate (S1P), mediates cell survival signaling. The enzyme sphingosine kinase produces S1P, and the activity of sphingosine kinase impacts the ability of cells to survive under stress and challenges. To examine the influence of sphingolipid metabolism, particularly enzymes regulating sphingosine and S1P, in mediating aging, neuronal function and stress response, we examined life history traits, locomotor capacities and heat stress responses of young and old animals using the model organism Caenorhabditis elegans...
2017: Frontiers in Genetics
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