Direct observation of stress response in Caenorhabditis elegans using a reporter transgene

Link, Christopher D.; Cypser, James R.; Johnson, Carolyn J.; Johnson, Thomas E.

doi:10.1379/1466-1268(1999)004<0235:doosri>2.3.co;2

Cited by 191 publications

(165 citation statements)

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“…To explore this possibility, we measured the effect of aip-1(RNAi) on the expression of two stress-inducible reporter genes: hsp-16 pr ::gfp, which reports on the activity of the heat-shock response (13), and sod-3 pr ::gfp, which reports on the levels of oxidative stress response (14). Both pathways were activated by arsenite in the control animals, as expected.…”

Section: Worm Aip-1 Is Required For Normal Lifespan and Resistance Tomentioning

confidence: 78%

Proteasomal adaptation to environmental stress links resistance to proteotoxicity with longevity in Caenorhabditis elegans

Yun¹,

Stanhill

Yun³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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The burden of protein misfolding is believed to contribute to aging. However, the links between adaptations to conditions associated with protein misfolding and resistance to the time-dependent attrition of cellular function remain poorly understood. We report that worms lacking aip-1, a homologue of mammalian AIRAP (arsenic-inducible proteasomal 19S regulatory particle-associated protein), are not only impaired in their ability to resist exposure to arsenite but also exhibit shortened lifespan and hypersensitivity to misfolding-prone proteins under normal laboratory conditions. Mammals have a second, constitutively expressed AIRAP-like gene (AIRAPL) that also encodes a proteasome-interacting protein, which shares with AIRAP the property of enhancing peptide accessibility to the proteasome's active site. Genetic rescue experiments suggest that features common to the constitutively expressed worm AIP-1 and mammalian AIRAPL (but missing in the smaller, arsenite-inducible AIRAP) are important to lifespan extension. In worms, a single AIRAP-related protein links proteasomal adaptation to environmental stress with resistance to both proteotoxic insults and maintenance of animal life span under normal conditions. aging ͉ chaperones ͉ environmental toxins ͉ protein degradation

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Section: Worm Aip-1 Is Required For Normal Lifespan and Resistance Tomentioning

confidence: 78%

Proteasomal adaptation to environmental stress links resistance to proteotoxicity with longevity in Caenorhabditis elegans

Yun¹,

Stanhill

Yun³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…The reporter encodes no HSP-16.2 product itself, and GFP protein expressed via this construct has the same expression pattern as HSP-16.2, so that those worms with high GFP expression have a high HSP-16 expression, and worms with low GFP expression have a low HSP-16 expression (Link et al 1999). Consequently, the levels of GFP fluorescence and HSP-16.2 expression are strongly correlated in TJ375.…”

Section: Strains and Culture Conditionsmentioning

confidence: 99%

“…b Effect of GABA on the nose touch response. c Percent of shrinking response in GABA non-treated and treated worms exposed to H 2 O 2 (n = 90 assays per group, *P < 0.05) is more perceptible, although usually it can be seen in the entire worm (Link et al 1999).…”

Section: Picrotoxin Exposure Enhanced Hsp-162 Protein Expressionmentioning

confidence: 99%

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

Camargo

Elizalde

Trujillo

et al. 2016

Cell Stress and Chaperones

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The mechanisms underlying oxidative stress (OS) resistance are not completely clear. Caenorhabditis elegans (C. elegans) is a good organism model to study OS because it displays stress responses similar to those in mammals. Among these mechanisms, the insulin/IGF-1 signaling (IIS) pathway is thought to affect GABAergic neurotransmission. The aim of this study was to determine the influence of heat shock stress (HS) on GABAergic activity in C. elegans. For this purpose, we tested the effect of exposure to picrotoxin (PTX), gammaaminobutyric acid (GABA), hydrogen peroxide, and HS on the occurrence of a shrinking response (SR) after nose touch stimulus in N2 (WT) worms. Moreover, the effect of HS on the expression of UNC-49 (GABA A receptor ortholog) in the EG1653 strain and the effect of GABA and PTX exposure on HSP-16.2 expression in the TJ375 strain were analyzed. PTX 1 mM-or H 2 O 2 0.7 mM-exposed worms displayed a SR in about 80 % of trials. GABA exposure did not cause a SR. HS prompted the occurrence of a SR as did PTX 1 mM or H 2 O 2 0.7 mM exposure. In addition, HS increased UNC-49 expression, and PTX augmented HSP-16.2 expression. Thus, the results of the present study suggest that oxidative stress, through either H 2 O 2 exposure or application of heat shock, inactivates the GABAergic system, which subsequently would affect the oxidative stress response, perhaps by enhancing the activity of transcription factors DAF-16 and HSF-1, both regulated by the IIS pathway and related to hsp-16.2 expression.

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“…Our list of test toxicants will include several metals as well as a variety of widely used pesticides acting on different targets. Currently available stress-inducible reporter strains in C. elegans include: hsp-16.2 [36], sod-3, cep-1 [18], cyp-35A2 [37], gst-1 [38], mtl-1/ mtl-2 [6] and hsp-16.1 [39] strains. This range of reporters has been greatly expanded thanks to the Baillie group's pioneering genome-wide GFP reporter project [40] to include:-hsp-60, gst-4, sod-1/-2/-4, ctl-1/-2, skn-1, hsf-1, 4 P450 genes (cyp-29A2/-31A3/-34A9/-35A3) [37] and 3 glutathione peroxidase genes, plus genes involved in DNA repair.…”

Section: Experimental Approachmentioning

confidence: 99%

The Stress-Response Network in Animals: Proposals to Develop a Predictive Mathematical Model

Pomerai¹,

Madhamshettiwar²,

Anbalagan³

et al. 2009

TOTOXIJ

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Abstract:Increasing evidence indicates that numerous genetic pathways responding to environmental stress in animals are regulated co-ordinately as well as independently. These stress-response systems should therefore be viewed in holistic terms as a network. As such, their behaviour is susceptible to mathematical modelling using a systems biology approach. This review outlines relevant evidence and describes a newly launched project to develop just such a model using stressresponse data from multiple transgenic strains of C. elegans and D. melanogaster. We hope that our eventual model will be capable of predicting the effects of simple stressor mixtures with reasonable accuracy. To maximise the effectiveness and scope of this model, we appeal for help from colleagues to share reagents and data relevant to this project. We also present preliminary data where RNA interference has implicated the key transcription factor DAF-16 in an unexpected upregulation of cyp-34A9 reporter expression by high cadmium. STRESS RESPONSES AND MIXTURE TOXICITYIn multicellular organisms, the defensive cellular responses evoked by environmental stresses do not result from simple linear pathways, but rather from a network of interlinked pathways with multiple outputs. This makes it difficult to predict the biological effects of multiple stressors acting together, even though this is the normal situation for industrial pollution of soil or water, where several different contaminants are usually present together. There are few studies and no useful predictive models describing the molecular responses of multicellular organisms to several toxicants acting in concert. This is essentially a systems biology problem, requiring integration of complex molecular and toxicological information. Under the auspices of a Major Award from the UK-India Education and Research Initiative (UK-IERI), we intend to develop an in silico model describing the principal elements of a consensus stress response network (SRN) and its in vivo responses to single stressors, using data from two invertebrate model systems, the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. This model will be used to predict the likely SRN responses to stressor mixtures, and such predictions will then be tested experimentally in both species so that the model can be refined accordingly. Since the SRN core pathways are highly conserved among animal taxa, general features of this model should find wider application in ecotoxi-*Address correspondence to this author at the School of Biology, Nottingham University, Nottingham NG7 2RD, UK; Tel: (0044) 115 951 3250; Fax: (0044) 115 951 3251; E-mail: david.depomerai@nottingham.ac.uk cology. The dynamic aspects of this model, and in particular its ability to integrate multiple toxicant inputs for predicting likely SRN outputs, distinguish this from a simple map of the regulatory gene-circuits comprising the SRN. THE C. ELEGANS STRESS-RESPONSE NETWORKThe free-living soil nematode, C. elegans, is particularly suitable fo...

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Direct observation of stress response in Caenorhabditis elegans using a reporter transgene

Cited by 191 publications

References 0 publications

Proteasomal adaptation to environmental stress links resistance to proteotoxicity with longevity in Caenorhabditis elegans

Proteasomal adaptation to environmental stress links resistance to proteotoxicity with longevity in Caenorhabditis elegans

Inactivation of GABAA receptor is related to heat shock stress response in organism model Caenorhabditis elegans

The Stress-Response Network in Animals: Proposals to Develop a Predictive Mathematical Model

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