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C elegans aging

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https://www.readbyqxmd.com/read/28632756/identification-of-atf-7-and-the-insulin-signaling-pathway-in-the-regulation-of-metallothionein-in-c-elegans-suggests-roles-in-aging-and-reactive-oxygen-species
#1
Julie A Hall, Matthew K McElwee, Jonathan H Freedman
It has been proposed that aging results from the lifelong accumulation of intracellular damage via reactions with reactive oxygen species (ROS). Metallothioneins are conserved cysteine-rich proteins that function as efficient ROS scavengers and may affect longevity. To better understand mechanisms controlling metallothionein expression, the regulatory factors and pathways that controlled cadmium-inducible transcription of the C. elegans metallothionein gene, mtl-1, were identified. The transcription factor ATF-7 was identified in both ethylmethanesulfonate mutagenesis and candidate gene screens...
2017: PloS One
https://www.readbyqxmd.com/read/28627510/glycogen-controls-caenorhabditis-elegans-lifespan-and-resistance-to-oxidative-stress
#2
Ivan Gusarov, Bibhusita Pani, Laurent Gautier, Olga Smolentseva, Svetlana Eremina, Ilya Shamovsky, Olga Katkova-Zhukotskaya, Alexander Mironov, Evgeny Nudler
A high-sugar diet has been associated with reduced lifespan in organisms ranging from worms to mammals. However, the mechanisms underlying the harmful effects of glucose are poorly understood. Here we establish a causative relationship between endogenous glucose storage in the form of glycogen, resistance to oxidative stress and organismal aging in Caenorhabditis elegans. We find that glycogen accumulated on high dietary glucose limits C. elegans longevity. Glucose released from glycogen and used for NADPH/glutathione reduction renders nematodes and human hepatocytes more resistant against oxidative stress...
June 19, 2017: Nature Communications
https://www.readbyqxmd.com/read/28622510/microbial-genetic-composition-tunes-host-longevity
#3
Bing Han, Priya Sivaramakrishnan, Chih-Chun J Lin, Isaiah A A Neve, Jingquan He, Li Wei Rachel Tay, Jessica N Sowa, Antons Sizovs, Guangwei Du, Jin Wang, Christophe Herman, Meng C Wang
Homeostasis of the gut microbiota critically influences host health and aging. Developing genetically engineered probiotics holds great promise as a new therapeutic paradigm to promote healthy aging. Here, through screening 3,983 Escherichia coli mutants, we discovered that 29 bacterial genes, when deleted, increase longevity in the host Caenorhabditis elegans. A dozen of these bacterial mutants also protect the host from age-related progression of tumor growth and amyloid-beta accumulation. Mechanistically, we discovered that five bacterial mutants promote longevity through increased secretion of the polysaccharide colanic acid (CA), which regulates mitochondrial dynamics and unfolded protein response (UPR(mt)) in the host...
June 15, 2017: Cell
https://www.readbyqxmd.com/read/28622501/microbiome-and-longevity-gut-microbes-send-signals-to-host-mitochondria
#4
Jan Gruber, Brian K Kennedy
The microbiome has emerged as a major determinant of the functioning of host organisms, affecting both health and disease. Here, Han et al. use the workhorse of aging research, C. elegans, to identify specific mechanisms by which gut bacteria influence mitochondrial dynamics and aging, a first step toward analogous manipulations to modulate human aging.
June 15, 2017: Cell
https://www.readbyqxmd.com/read/28620943/drug-repurposing-for-aging-research-using-model-organisms
#5
Matthias Ziehm, Satwant Kaur, Dobril K Ivanov, Pedro J Ballester, David Marcus, Linda Partridge, Janet M Thornton
Many increasingly prevalent diseases share a common risk factor: age. However, little is known about pharmaceutical interventions against aging, despite many genes and pathways shown to be important in the aging process and numerous studies demonstrating that genetic interventions can lead to a healthier aging phenotype. An important challenge is to assess the potential to repurpose existing drugs for initial testing on model organisms, where such experiments are possible. To this end, we present a new approach to rank drug-like compounds with known mammalian targets according to their likelihood to modulate aging in the invertebrates Caenorhabditis elegans and Drosophila...
June 16, 2017: Aging Cell
https://www.readbyqxmd.com/read/28612944/the-skn-1-nrf2-transcription-factor-can-protect-against-oxidative-stress-and-increase-lifespan-in-c-%C3%A2-elegans-by-distinct-mechanisms
#6
Jennifer M A Tullet, James W Green, Catherine Au, Alexandre Benedetto, Maximillian A Thompson, Emily Clark, Ann F Gilliat, Adelaide Young, Kathrin Schmeisser, David Gems
In C. elegans, the skn-1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn-1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN-1 on Oxr and longevity can be dissociated. We also establish that skn-1 expression can be activated by the DAF-16/FoxO transcription factor, another central regulator of growth, metabolism, and aging...
June 14, 2017: Aging Cell
https://www.readbyqxmd.com/read/28602540/deficiencies-in-mitochondrial-dynamics-sensitize-caenorhabditis-elegans-to-arsenite-and-other-mitochondrial-toxicants-by-reducing-mitochondrial-adaptability
#7
Anthony L Luz, Tewodros R Godebo, Latasha L Smith, Tess C Leuthner, Laura L Maurer, Joel N Meyer
Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases...
June 8, 2017: Toxicology
https://www.readbyqxmd.com/read/28600327/the-oxidative-stress-response-in-caenorhabditis-elegans-requires-the-gata-transcription-factor-elt-3-and-skn-1-nrf2
#8
Queenie Hu, Dayana R D'Amora, Lesley T MacNeil, Albertha J M Walhout, Terrance J Kubiseski
Cellular damage caused by reactive oxygen species (ROS) is believed to be a major contributor to age-associated diseases. Previously, we characterized the C. elegans Brap2 ortholog (BRAP-2) and found that it is required to prevent larval arrest in response to elevated levels of oxidative stress. Here, we report that C. elegans brap-2 mutants display increased expression of SKN-1-dependent phase II detoxification enzymes that is dependent on PMK-1 (a p38 MAP kinase C. elegans ortholog). An RNAi screen was conducted using a transcription factor library to identify genes required for increased expression of the SKN-1 target gst-4 in brap-2 mutants...
June 9, 2017: Genetics
https://www.readbyqxmd.com/read/28576774/aff-1-fusogen-can-rejuvenate-the-regenerative-potential-of-adult-dendritic-trees-via-self-fusion
#9
Veronika Kravtsov, Meital Oren-Suissa, Benjamin Podbilewicz
The aging brain undergoes structural changes, affecting brain homeostasis, neuronal function and consequently cognition. The complex architecture of dendritic arbors poses a challenge to understanding age-dependent morphological alterations, behavioral plasticity and remodeling following brain injury. Here, we use the PVD polymodal neurons of C. elegans as a model to study how aging affects neuronal plasticity. Using confocal live imaging of C. elegans PVD neurons, we demonstrate age-related progressive morphological alterations of intricate dendritic arbors...
June 2, 2017: Development
https://www.readbyqxmd.com/read/28567542/current-perspective-in-the-discovery-of-anti-aging-agents-from-natural-products
#10
REVIEW
Ai-Jun Ding, Shan-Qing Zheng, Xiao-Bing Huang, Ti-Kun Xing, Gui-Sheng Wu, Hua-Ying Sun, Shu-Hua Qi, Huai-Rong Luo
Aging is a process characterized by accumulating degenerative damages, resulting in the death of an organism ultimately. The main goal of aging research is to develop therapies that delay age-related diseases in human. Since signaling pathways in aging of Caenorhabditis elegans (C. elegans), fruit flies and mice are evolutionarily conserved, compounds extending lifespan of them by intervening pathways of aging may be useful in treating age-related diseases in human. Natural products have special resource advantage and with few side effect...
May 31, 2017: Natural Products and Bioprospecting
https://www.readbyqxmd.com/read/28567012/age-dependent-protein-aggregation-initiates-amyloid-%C3%AE-aggregation
#11
Nicole Groh, Anika Bühler, Chaolie Huang, Ka Wan Li, Pim van Nierop, August B Smit, Marcus Fändrich, Frank Baumann, Della C David
Aging is the most important risk factor for neurodegenerative diseases associated with pathological protein aggregation such as Alzheimer's disease. Although aging is an important player, it remains unknown which molecular changes are relevant for disease initiation. Recently, it has become apparent that widespread protein aggregation is a common feature of aging. Indeed, several studies demonstrate that 100s of proteins become highly insoluble with age, in the absence of obvious disease processes. Yet it remains unclear how these misfolded proteins aggregating with age affect neurodegenerative diseases...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28546536/a-sensitive-mass-spectrometry-platform-identifies-metabolic-changes-of-life-history-traits-in-c-elegans
#12
Arwen W Gao, Iliana A Chatzispyrou, Rashmi Kamble, Yasmine J Liu, Katharina Herzog, Reuben L Smith, Henk van Lenthe, Martin A T Vervaart, Arno van Cruchten, Angela C Luyf, Antoine van Kampen, Mia L Pras-Raves, Frédéric M Vaz, Riekelt H Houtkooper
Abnormal nutrient metabolism is a hallmark of aging, and the underlying genetic and nutritional framework is rapidly being uncovered, particularly using C. elegans as a model. However, the direct metabolic consequences of perturbations in life history of C. elegans remain to be clarified. Based on recent advances in the metabolomics field, we optimized and validated a sensitive mass spectrometry (MS) platform for identification of major metabolite classes in worms and applied it to study age and diet related changes...
May 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28545550/genetic-variation-in-neurodegenerative-diseases-and-its-accessibility-in-the-model-organism-caenorhabditis-elegans
#13
REVIEW
Yiru Anning Wang, Jan Edward Kammenga, Simon Crawford Harvey
BACKGROUND: Neurodegenerative diseases (NGDs) such as Alzheimer's and Parkinson's are debilitating and largely untreatable conditions strongly linked to age. The clinical, neuropathological, and genetic components of NGDs indicate that neurodegeneration is a complex trait determined by multiple genes and by the environment. MAIN BODY: The symptoms of NGDs differ among individuals due to their genetic background, and this variation affects the onset and progression of NGD and NGD-like states...
May 25, 2017: Human Genomics
https://www.readbyqxmd.com/read/28544360/impairment-of-insulin-signalling-in-peripheral-tissue-fails-to-extend-murine-lifespan
#14
Troy L Merry, Doreen Kuhlow, Beate Laube, Doris Pöhlmann, Andreas F H Pfeiffer, C Ronald Kahn, Michael Ristow, Kim Zarse
Impaired insulin/IGF1 signalling has been shown to extend lifespan in model organisms ranging from yeast to mammals. Here we sought to determine the effect of targeted disruption of the insulin receptor (IR) in non-neuronal tissues of adult mice on the lifespan. We induced hemizygous (PerIRKO(+/-) ) or homozygous (PerIRKO(-/-) ) disruption of the IR in peripheral tissue of 15-weeks-old mice using a tamoxifen-inducible Cre transgenic mouse with only peripheral tissue expression, and subsequently monitored glucose metabolism, insulin signalling and spontaneous death rates over 4 years...
May 22, 2017: Aging Cell
https://www.readbyqxmd.com/read/28544111/kallistatin-reduces-vascular-senescence-and-aging-by-regulating-microrna-34a-sirt1-pathway
#15
Youming Guo, Pengfei Li, Lin Gao, Jingmei Zhang, Zhirong Yang, Grant Bledsoe, Eugene Chang, Lee Chao, Julie Chao
Kallistatin, an endogenous protein, protects against vascular injury by inhibiting oxidative stress and inflammation in hypertensive rats and enhancing the mobility and function of endothelial progenitor cells (EPCs). We aimed to determine the role and mechanism of kallistatin in vascular senescence and aging using cultured EPCs, streptozotocin (STZ)-induced diabetic mice, and Caenorhabditis elegans (C. elegans). Human kallistatin significantly decreased TNF-α-induced cellular senescence in EPCs, as indicated by reduced senescence-associated β-galactosidase activity and plasminogen activator inhibitor-1 expression, and elevated telomerase activity...
May 24, 2017: Aging Cell
https://www.readbyqxmd.com/read/28537553/longitudinal-imaging-of-caenorhabditis-elegans-in-a-microfabricated-device-reveals-variation-in-behavioral-decline-during-aging
#16
Matthew A Churgin, Sang-Kyu Jung, Chih-Chieh Yu, Xiangmei Chen, David M Raizen, Christopher Fang-Yen
The roundworm C. elegans is a mainstay of aging research due to its short lifespan and easily manipulable genetics. Current, widely used methods for long-term measurement of C. elegans are limited by low throughput and the difficulty of performing longitudinal monitoring of aging phenotypes. Here we describe the WorMotel, a microfabricated device for long-term cultivation and automated longitudinal imaging of large numbers of C. elegans confined to individual wells. Using the WorMotel, we find that short-lived and long-lived strains exhibit patterns of behavioral decline that do not temporally scale between individuals or populations, but rather resemble the shortest and longest lived individuals in a wild type population...
May 24, 2017: ELife
https://www.readbyqxmd.com/read/28537485/a-nad-parp1-sirt1-axis-in-aging
#17
Andrew R Mendelsohn, James Larrick
NAD+ levels decline with age in diverse animals from C. elegans to mice. Raising NAD+ levels by dietary supplementation with NAD+ precursors NR or NMN improves mitochondrial function and muscle, neural and melanocyte stem cell function in mice as well as increasing murine lifespan. Decreased NAD+ levels with age reduces SIRT1 function and reduces the mitochondrial unfolded protein response, which can be overcome by NR supplementation. Decreased NAD+ levels cause NAD+-binding protein DCB1 to form a complex with PARP1, inhibiting PARP catalytic activity...
May 24, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/28524858/caspase-dependent-non-apoptotic-processes-in-development
#18
REVIEW
Yu-Ichiro Nakajima, Erina Kuranaga
Caspases are at the core of executing apoptosis by orchestrating cellular destruction with proteolytic cascades. Caspase-mediated proteolysis also controls diverse nonlethal cellular activities such as proliferation, differentiation, cell fate decision, and cytoskeletal reorganization. During the last decade or so, genetic studies of Drosophila have contributed to our understanding of the in vivo mechanism of the non-apoptotic cellular responses in developmental contexts. Furthermore, recent studies using C...
May 19, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28503972/molecular-mechanisms-of-anti-oxidant-and-anti-aging-effects-induced-by-convallatoxin-in-caenorhabditis-elegans
#19
Jia Xu, Youming Guo, Tianzhuo Sui, Qifei Wang, Yue Zhang, Ruining Zhang, Mingyang Wang, Shuwen Guan, Liping Wang
Convallatoxin is widely used as a cardiac glycoside in acute and chronic congestive heart-failure and paroxysmal tachycardia, with many effects and underlying protective mechanisms on inflammation and cellular proliferation. However, convallatoxin has not been investigated in its antioxidant effects and lifespan extension in Caenorhabditis elegans. In this study, we found that convallatoxin (20 μM) could significantly prolong the lifespan of wild-type C. elegans up to 16.3% through daf-16, but not sir-2.1 signaling and increased thermotolerance and resistance to paraquat-induced oxidative stress...
May 14, 2017: Free Radical Research
https://www.readbyqxmd.com/read/28493873/modeling-of-a-negative-feedback-mechanism-explains-antagonistic-pleiotropy-in-reproduction-in-domesticated-caenorhabditis-elegans-strains
#20
Edward E Large, Raghavendra Padmanabhan, Kathie L Watkins, Richard F Campbell, Wen Xu, Patrick T McGrath
Most biological traits and common diseases have a strong but complex genetic basis, controlled by large numbers of genetic variants with small contributions to a trait or disease risk. The effect-size of most genetic variants is not absolute and is instead dependent upon multiple factors such as the age and genetic background of an organism. In order to understand the mechanistic basis of these changes, we characterized heritable trait differences between two domesticated strains of C. elegans. We previously identified a major effect locus, caused in part by a mutation in a component of the NURF chromatin remodeling complex, that regulates reproductive output in an age-dependent manner...
May 2017: PLoS Genetics
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