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Transcriptional response to MnSOD over-expression in Drosophila melanogaster

ABSTRACT: Profiled the transcriptional response to over-expression Manganese-SOD (MnSOD) in adult Drosophila. A doxycycline-regulated system was employed to induce MnSOD over-expression, resulting in mean and maximal lifespan increases of ~ 20%. Examination of the genome-wide response to this lifespan intervention provided key insights into the molecular basis of aging. Keywords: genetic modification; MnSOD over-expression

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE7159 | GEO | 2008/01/01

SECONDARY ACCESSION(S): PRJNA98161

REPOSITORIES: GEO

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Transcription profiling of Drosophila overexpressing MnSOD

Project description:Profiled the transcriptional response to over-expression Manganese-SOD (MnSOD) in adult Drosophila. A doxycycline-regulated system was employed to induce MnSOD over-expression, resulting in mean and maximal lifespan increases of ~ 20%. Examination of the genome-wide response to this lifespan intervention provided key insights into the molecular basis of aging. Experiment Overall Design: 20 Affymetrix DrosGenome1 arrays were employed with four replicates for each of five conditions. Cohorts of treated and untreated MnSOD transgenic flies were sampled at the same chronological age (~50% survival of -DOX flies, day 73) as well as, at the same physiological age (~50% survival for +DOX and -DOX flies, day 83 and day 73, respectively). The effect of DOX was controlled for by sampling control flies treated with or without DOX at the same chronological age (~50% survival of -DOX flies, day 78).

2008-06-15 | E-GEOD-7159 | biostudies-arrayexpress

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Project description:Transcriptional response to MnSOD over-expression in Drosophila melanogaster

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Drosophila melanogaster transcriptional profiling over life span: Indy vs. Controls

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RNA-sequencing of C.elegans isp-1 mutant and superoxide dismutase-isp-1 double mutants

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Drosophila melanogaster transcriptional profiling over life span: Indy vs. Controls

Project description:Transcriptional profiling of Indy long lived flies and controls over the course of their entire lifespan. Mutations in the Indy gene extend life span in Drosophila melanogaster. This study investigates the changes in gene expression over time in Indy206 flies heterozygous over Canton-S (Indy206/CS) and compares them to genetically matched heterozygous controls (2216/CS). Samples from both fly strains were collected at age: 5, 10, 20, 30, 40, 50, 70 and 80. mRNA samples were collected from the head and thorax of Indy206 and genetically matched control male adult flies at day 5, and every 10 days from day 10 to day 80 (day 60 excluded) and hybridized to two-color microarrays

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SRT2104 extends survival of male mice on a standard diet and preserves bone and muscle mass

Project description:Increased expression of SIRT1 extends the lifespan of lower organisms and delays the onset of age-related diseases in mammals. Here, we show that SRT2104, a synthetic small molecule activator of SIRT1, extends both mean and maximal lifespan of mice fed a standard diet. This is accompanied by improvements in health, including enhanced motor coordination, performance, bone mineral density and insulin sensitivity associated with higher mitochondrial content and decreased inflammation. Short-term SRT2104 treatment preserves bone and muscle mass in an experimental model of atrophy. These results demonstrate it is possible to design a small molecule that can slow aging and delay multiple age-related diseases in mammals, supporting the therapeutic potential of SIRT1 activators in humans. Key words: Sirtuins, lifespan, healthspan, osteoporosis, muscle wasting, inflammation

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Project description:Primary bile acids are produced in the liver whereas secondary bile acids such as lithocholic acid (LCA) are generated by gut bacteria from primary bile acids that escape the ileal absorption. Besides their well-known function as detergents in lipid digestion, bile acids are important signaling molecules mediating effects on the host’s metabolism. As energy metabolism is closely linked to aging and longevity we supplemented fruit flies (Drosophila melanogaster) with 50 µmol/l LCA either for 30 days or throughout their lifetime. LCA supplementation resulted in a significant induction of the mean (+12 days), median (+10 days) and maximum lifespan (+ 11 days) in comparison to untreated control flies. This lifespan extension was accompanied by an induction of spargel (srl), the fly homolog of mammalian PPARG co-activator 1a(PGC1A. In srl mutant flies, LCA failed to induce longevity emphasizing the essential role of srl in the observed lifespan extension. In addition, the administration of antibiotics to wild type flies abrogated LCA-mediated effects on both lifespan and srl expression, suggesting a substantial contribution of the intestinal microbiota to the LCA-induced longevity. In the present study, we show that the secondary bile acid LCA significantly induced the mean, the median and the maximum survival in Drosophila melanogaster. Our data suggest that besides an up-regulation of the PGC1a-homolog srl unidentified alterations in the structure or metabolism of gut microbiota contribute to the longevity effect of LCA.

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Comparison of hepatic gene expression between short-term calorie restricted wild-type and Dgat1 deficient middle-aged female mice

Project description:Leanness is associated with increased lifespan and is linked to favorable metabolic conditions promoting life extension. We show here that deficiency of the lipid synthesis enzyme acyl CoA:diacylglycerol acyltransferase 1 (DGAT1), which reduces body fat in mice, promotes longevity. Female DGAT1-deficient mice were protected from age-related increases in body fat, non-adipose tissue triglycerides, and markers of inflammation in white adipose tissue. These metabolic changes were accompanied by an increased mean and maximal lifespan of ~25% and ~10%, respectively. The gene expression profile of DGAT1-deficient mice was not highly correlated with calorie restriction of sex and age matched wild-type littermates. Our findings indicate that loss of DGAT1-mediated lipid synthesis results in leanness, protects against age-related metabolic consequences, and thus extends longevity.

2012-02-09 | GSE26267 | GEO

RNA microarray studies of aspirin's effect on MnSOD-deficient mutant [EG110, (MT)] and wild-type [EG103, (WT)] Saccharomyces cerevisiae yeast cells

Project description:Non-steroidal anti-inflammatory drugs, principally aspirin (acetylsalicylic acid, ASA), have anti-neoplastic properties, as shown by epidemiological studies on colorectal cancer and many other types of tumours. The chemopreventive and anti-proliferative properties of aspirin towards tumour cells have been shown to be due to the induction of programmed cell death such as apoptosis. Yeast cells are among the experimental models used extensively for the study of oxidative stress and apoptosis in living organisms because yeast, such as S. cerevisiae, retains many of the core eukaryotic cellular processes, including the hallmarks of eukaryotic apoptosis. An important contribution of our previous work has been the clarification of the critical defensive role of the antioxidant mitochondrial enzyme manganese superoxide dismutase (MnSOD) against apoptosis, confirmed to be the attenuation of aspirin-induced superoxide radical accumulation in the yeast mitochondria (Farrugia et al. (2013) FEMS Yeast Res 13, 755-768). To study the possible differential expression of gene transcripts in relation to the induction of apoptosis by aspirin, we used gene expression profiling by means of GeneChip® Microarray Technology (Affymetrix®). The yeast strains considered for this study included (1) the wild type strain S. cerevisiae EG103, which contains both MnSOD and cytosolic copper, zinc superoxide dismutase (CuZnSOD) and (2) the redox-compromised MnSOD-deficient S. cerevisiae EG110 strain. [This work was financed by the Malta Council for Science and Technology through the R&I Technology Development Programme (Project R&I-2015-001)].

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