Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of Drosophila overexpressing MnSOD

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. 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).

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Diana Abdueva

PROVIDER: E-GEOD-7159 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Publications

Transcriptional profiling of MnSOD-mediated lifespan extension in Drosophila reveals a species-general network of aging and metabolic genes.

Curtis Christina C Landis Gary N GN Folk Donna D Wehr Nancy B NB Hoe Nicholas N Waskar Morris M Abdueva Diana D Skvortsov Dmitriy D Ford Daniel D Luu Allan A Badrinath Ananth A Levine Rodney L RL Bradley Timothy J TJ Tavaré Simon S Tower John J

Genome biology 20070101 12

<h4>Background</h4>Several interventions increase lifespan in model organisms, including reduced insulin/insulin-like growth factor-like signaling (IIS), FOXO transcription factor activation, dietary restriction, and superoxide dismutase (SOD) over-expression. One question is whether these manipulations function through different mechanisms, or whether they intersect on common processes affecting aging.<h4>Results</h4>A doxycycline-regulated system was used to over-express manganese-SOD (MnSOD) ...[more]

PMID: 18067683

Similar Datasets

Project description:Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic JAK-STAT activation, reduced insulin sensitivity and hyperglycaemia, and a shorter lifespan. Drosophila macrophages scavenged lipids and produced the type 1 cytokine upd3, in a scavenger-receptor (croquemort) and JNK-dependent manner. Genetic depletion of macrophages, or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-M-NM-:B signalling made no contribution to the phenotype observed. These results identify an evolutionarily conserved M-bM-^@M-^Xscavenger receptor-JNK-Type 1 cytokineM-bM-^@M-^Y cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic JAK-STAT activation, reduced insulin sensitivity and hyperglycaemia, and a shorter lifespan. Drosophila macrophages scavenged lipids and produced the type 1 cytokine upd3, in a scavenger-receptor (croquemort) and JNK-dependent manner. Genetic depletion of macrophages, or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-M-NM-:B signalling made no contribution to the phenotype observed. These results identify an evolutionarily conserved M-bM-^@M-^Xscavenger receptor-JNK-Type 1 cytokineM-bM-^@M-^Y cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway 5 biological samples were FACS-sorted from different batches of Drosophila melanogaster males after 30 days on 15% lipid enriched diet (n=5) and control diet (n=5)

Dataset Information

Transcription profiling of Drosophila overexpressing MnSOD

Publications

Transcriptional profiling of MnSOD-mediated lifespan extension in Drosophila reveals a species-general network of aging and metabolic genes.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets