| Citation | Park SK, Tedesco PM, Johnson TE. Oxidative stress and longevity in Caenorhabditis elegans as mediated by SKN-1. Aging Cell, 2009. |
| PubMed ID | 19627265 |
| Short Description | Oxidative stress and longevity in Caenorhabditis elegans as mediated by SKN-1. GEO Record: GSE9301 Platform: GPL200 Download gene-centric, log2 transformed data: WBPaper00034757.ce.mr.csv |
| # of Conditions | 11 |
Full Description
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Oxidative stress has been hypothesized to play a role in normal aging. The response to oxidative stress is regulated by the SKN-1 transcription factor, which also is necessary for intestinal development in Caenorhabditis elegans. Almost a thousand genes including the antioxidant and heat-shock responses, as well as genes responsible for xenobiotic detoxification were induced by the oxidative stress which was found using transcriptome analysis. There were also 392 down-regulated genes including many involved in metabolic homeostasis, organismal development, and reproduction. Many of these oxidative stress-induced transcriptional changes are dependent on SKN-1 action; the induction of the heat-shock response is not. When RNAi to inhibit genes was used, most had no effect on either resistance to oxidative stress or longevity; however two SKN-1-dependent genes, nlp-7 and cup-4, that were up-regulated by oxidative stress were found to be required for resistance to oxidative stress and for normal lifespan. nlp-7 encodes a neuropeptide-like protein, expressed in neurons, while cup-4 encodes a coelomocyte-specific, ligand-gated ion channel. RNAi of nlp-7 or cup-4 increased sensitivity to oxidative stress and reduced lifespan. Among down-regulated genes, only inhibition of ent-1, a nucleoside transporter, led to increased resistance to oxidative stress; inhibition had no effect on lifespan. In contrast, RNAi of nhx-2, a Na(+)/H(+) exchanger, extended lifespan significantly without affecting sensitivity to oxidative stress. These findings showed that a transcriptional shift from growth and maintenance towards the activation of cellular defense mechanisms was caused by the oxidative stress; many of these transcriptional alterations are SKN-1 dependent. Experimental Details: WBPaper00034757:control_no_stress_1 WBPaper00034757:control_no_stress_2 WBPaper00034757:control_no_stress_3 WBPaper00034757:control_no_stress_4 WBPaper00034757:oxidative_stress_1 WBPaper00034757:oxidative_stress_2 WBPaper00034757:oxidative_stress_3 WBPaper00034757:oxidative_stress_4 WBPaper00034757:skn-1_RNAi_oxidative_stress_1 WBPaper00034757:skn-1_RNAi_oxidative_stress_2 WBPaper00034757:skn-1_RNAi_oxidative_stress_3. |
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