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Resveratrol treatment of daf-16 mutant C. elegans

ABSTRACT: Eggs were isolated by hypochlorite treatment and allowed to hatch in the absence of food as L1 stage arrested worms in S-buffer. Worms were then transferred to large plates containing NGM alone or NGM+ resveratrol and allowed to grow till young adult stage (ca 40 hours). Worms were harvested and total RNA extracted using trizol reagent. Poly-A+ RNA was isolated using Qiagen midi-prep kit and used for microarray hybridization. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Resveratrol Keywords: compound_treatment_design

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE4093 | GEO | 2006/01/25

SECONDARY ACCESSION(S): PRJNA104889

REPOSITORIES: GEO

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N2 worms treated with Resveratrol

Project description:Eggs were isolated by hypochlorite treatment and allowed to hatch in the absence of food as L1 stage arrested worms in S-buffer. Worms were then transferred to large plates containing NGM alone or NGM+ resveratrol and allowed to grow till young adult stage (ca 40 hours). Worms were harvested and total RNA extracted using Trizol reagent. Poly-A+ RNA was isolated using Qiagen midi-prep kit and used for microarray hybridization. A compound treatment design type is where the response to administration of a compound or chemical (including biological compounds such as hormones) is assayed. Compound Based Treatment: Resveratrol Keywords: compound_treatment_design

2006-01-25 | GSE4094 | GEO

Resveratrol treatment of daf-16 mutant C. elegans

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2006-01-24 | E-GEOD-4093 | biostudies-arrayexpress

N2 worms treated with Resveratrol

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Transcription profiling of C. elegans IG274 wt frIs7 and IG339 nipi-1(fr1) frIs7 after infection with Dreshmeria coniosporia

Project description:1.Sample Growth Conditions protocols Eggs from IG274 wt; frIs7 and IG339 nipi-1(fr1); frIs7 worms cultivated at 25ÃÂ°C were allowed to hatch in the absence of food at 25ÃÂ°C for 16 hours. Synchronised larvae were transferred to NGM agar plates lawned with OP50 and cultivated at 25°C for 48 hours. 2.Sample Treatment protocols Synchronised IG274 wt; frIs7 and IG339 nipi-1(fr1); frIs7 worms at the young L4 stage were infected with freshly harvested spores of Dreshmeria coniosporia. After 24 hours at 25°C, the worms were collected into trizol for further RNA extraction. Controls worms were non infected.

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A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span

Project description:This SuperSeries is composed of the following subset Series: GSE4093: Resveratrol treatment of daf-16 mutant C. elegans GSE4094: N2 worms treated with Resveratrol GSE4095: Sir-2.1 low copy transgenic Abstract: C. elegans SIR-2.1, a member of the Sir-2 family of NAD(+)-dependent protein deacetylases, has been shown to regulate nematode aging via the insulin/IGF pathway transcription factor daf-16. Treatment of C. elegans with the small molecule resveratrol, however, extends life span in a manner fully dependent upon sir-2.1, but independent of daf-16. Microarray analysis of worms treated with resveratrol demonstrates the transcriptional induction of a family of genes encoding prion-like glutamine/asparagine-rich proteins involved in endoplasmic reticulum (ER) stress response to unfolded proteins. RNA interference of abu-11, a member of this ER stress gene family, abolishes resveratrol-mediated life span extension, and overexpression of abu-11 extends the life span of transgenic animals. Furthermore, SIR-2.1 normally represses transcription of abu-11 and other ER stress gene family members, indicating that resveratrol extends life span by inhibiting sir-2.1-mediated repression of ER stress genes. Our findings demonstrate that abu-11 and other members of its ER stress gene family are positive determinants of C. elegans life span. Refer to individual Series

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A Chinese herbal formula, Gengnianchun, ameliorates β-amyloid peptide toxicity in a Caenorhabditis elegans model of Alzheimer’s disease

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