title: Effects of sod gene overexpression and deletion mutation on the expression profiles of reporter genes of major detoxification pathways in Caenorhabditis elegans.
abstract: Reactive oxygen species have long been considered a major cause of aging. However, previous work showed that loss of superoxide dismutase (SOD) only weakly affects lifespan of Caenorhabditis elegans. Here, we examined the impact of sod gene deletion and overexpression on the mRNA levels of the remaining sod genes and other detoxification genes. We detected no compensatory upregulation of other sod genes in any of the sod deletion mutants in both wild-type and daf-2(m577) genetic backgrounds when L4 larvae were shifted from 17 to 24 degrees C, and harvested as young adults. Elimination of MnSOD increased transcription of SKN-1 regulated genes and reduced transcription of multiple DAF-16 targets. Loss of the major Cu/ZnSOD isoform SOD-1 caused enhanced expression of subsets of both SKN-1 and DAF-16 targets when the animals were grown continuously at 24 degrees C, and strong overexpression of sod-1 induced a compensatory decrease in all tested SKN-1 regulated gst genes. When combined, these results suggest that low cytosolic SOD may activate SKN-1 signaling, whereas high levels may be repressive. Overall, our results suggest that sod gene manipulation causes complex, combinatorial regulation of expression of individual targets of stress sensitive transcription factors.
authors.affiliation: Laboratory for Aging Physiology and Molecular Evolution, Department of Biology, Ghent University, K.L. Ledeganckstraat 35, Ghent, Belgium. patricia.back@ugent.be
authors.forename: Patricia
authors.initials: P
authors.lastname: Back
authors.forename: Filip
authors.initials: F
authors.lastname: Matthijssens
authors.forename: Caroline
authors.initials: C
authors.lastname: Vlaeminck
authors.forename: Bart P
authors.initials: BP
authors.lastname: Braeckman
authors.forename: Jacques R
authors.initials: JR
authors.lastname: Vanfleteren
mesh_terms: D000375:Aging / Q000235:genetics / Q000378:metabolism; D000818:Animals; D030801:Animals, Genetically Modified; D001665:Binding Sites / Q000235:genetics; D017173:Caenorhabditis elegans / Q000201:enzymology* / Q000235:genetics* / Q000254:growth & development; D029742:Caenorhabditis elegans Proteins / Q000235:genetics* / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D051858:Forkhead Transcription Factors; D050980:GATA Transcription Factors / Q000378:metabolism; D017353:Gene Deletion; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental; D017238:Genes, Helminth; D017930:Genes, Reporter; D008658:Inactivation, Metabolic / Q000235:genetics / Q000502:physiology; D008136:Longevity / Q000235:genetics / Q000502:physiology; D009154:Mutation; D018384:Oxidative Stress; D011401:Promoter Regions, Genetic; D018510:RNA, Helminth / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D013482:Superoxide Dismutase / Q000235:genetics* / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D029742:Caenorhabditis elegans Proteins; D004268:DNA-Binding Proteins; D051858:Forkhead Transcription Factors; D050980:GATA Transcription Factors; D018510:RNA, Helminth; D012333:RNA, Messenger; D014157:Transcription Factors; C108831:daf-16 protein, C elegans; C118721:elt-3 protein, C elegans; C073702:skn-1 protein, C elegans; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1