Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB18504 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR582639.fastq.gz | Fastqsanger.gz | |||
| DRR582640.fastq.gz | Fastqsanger.gz | |||
| DRR582641.fastq.gz | Fastqsanger.gz | |||
| DRR582642.fastq.gz | Fastqsanger.gz | |||
| DRR582643.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptomics of Gcn5-knocked down larvae and epigenomics of Drosophila melanogaster larvae fed on a diet rich in oleic acid, valine and acetate
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Project description:PFJ (4 ml for a final concentration of 19,000 mg gallic acid equivalent (GAE) per kg diet or 0.86 mg GAE per kcal diet) was supplemented to larvae of fruit flies (Drosophila melanogaster) given a semi-purified diet to observe for possible effects on energy metabolism and lifespan. Larvae were used five days since the egg stage for gene expression studies. Results from the microarray data analysis carried out show that fruit fly larvae given PFJ had up-regulated transport and metabolic processes, while development and morphogenesis processes were down-regulated.
2017-01-06 | GSE93220 | GEO
Project description:PFJ (4 ml for a final concentration of 19,000 mg gallic acid equivalent (GAE) per kg diet or 0.86 mg GAE per kcal diet) was supplemented to larvae of fruit flies (Drosophila melanogaster) given a semi-purified diet to observe for possible effects on energy metabolism and lifespan. Fat bodies extracted from these larvae were used five days since the egg stage for gene expression studies. Results from the microarray data analysis carried out show that fruit fly larva fat bodies given PFJ had up-regulated heat shock protein genes, while cell cycle and growth genes were down-regulated.
2017-01-06 | GSE93221 | GEO
Project description:In this experiment, Drosophila melanogaster larvae were fed with Proline and Arginine compounds and showed a better tolerance to freezing compared to control larvae. Using a microarray approach, we investigated the alteration of transcriptome profiles in larvae fed with Proline or Arginine versus control larvae.
2019-01-01 | E-MTAB-3911 | biostudies-arrayexpress
Project description:We used microarrays to investigate the transcriptome of male flies exposed to either a rich or a poor nutrient environment during development. Further we investigated transcriptome of their offspring and grand-offspring also developed at poor or rich diet. The ability of organisms to cope with poor quality nutrition is essential for their persistence. For species with short generation time, the nutritional environments can transcend generations, making it beneficial for adults to prime their offspring to particular diets. However, our understanding of potential adaptive generational effects, including those of diet quality, is still very limited. Here we use the vinegar fly, Drosophila melanogaster, to investigate if females developing as larvae on a nutritionally poor diet produce offspring that are primed for nutrient deficiencies in the following generations. We found that females developed at low quality diets produced offspring, which at similarly low-quality diets had both increased egg-to-adult viability and starvation tolerance compared to females experiencing a nutrient rich diet in the previous generation. When testing the persistence of such generational priming, we found that just one generation of high-quality diet is sufficient to return performance to initial levels. A global transcriptomic profile analysis suggests that the observed phenotypic priming is not a constitutive transcriptomic adjustment, instead offspring appear primed to initiate an adaptive response only when exposed to low quality diets. Our results show that generational priming is likely an important adaptive mechanism of coping with transient nutritional fluctuations.
2023-07-12 | GSE236807 | GEO
Project description:Transfer RNAs (tRNAs) are vital in determining the specificity of translation. Mutations in tRNAs can result in the mis-incorporation of amino acids into nascent polypeptides in a process known as mistranslation. Here, our goal was to test the impacts of different types of mistranslation in the model organism Drosophila melanogaster, as impact of mistranslation depends on the type of amino acid substitution. We created two fly lines - one expressing a serine tRNA variant with valine anticodon and the other with a serine tRNA variant with a threonine anticodon. Using mass spectrometry, we measure the amount of mistranslation at various points in fly development.
2024-06-15 | PXD052492 | Pride
Project description:Dietary n-3 polyunsaturated fatty acids can reduce inflammation via a range of mechanisms. This study tested the effect of dietary eicosapentaenoic acid (EPA) on intestinal inflammation using interleukin-10 gene-deficient (Il10-/-) mice. Methods: At 35 days of age, 12 weaned Il10-/- and 12 C57 mice were randomly assigned to one of two modified AIN-76A diets, supplemented with 3.7% purified ethyl esters of either EPA (n-3) or oleic acid (OA, control). To identify genes relevant to colon inflammation, transcription profiling (microarrays and qRT-PCR) and bioinformatic analyses were used. Results: In this study, dietary EPA reversed the decrease in colon fatty acid β-oxidation gene expression observed in OA-fed Il10-/- compared to C57 mice. Il10-/- mice fed the OA diet showed decreased expression of antioxidant enzyme genes, as well as those involved in detoxification of xenobiotics, compared to C57 mice on the same diet. In contrast, dietary EPA increased the expression of these genes in Il10-/- mice. Conclusions: These data indicate that dietary EPA induced endogenous lipid oxidation which might have a potential anti-inflammatory effect on colon tissue. This is supported by the activation of the Ppara gene that regulates the expression of pro-inflammatory and immunomodulatory genes and proteins. Experiment Overall Design: The diet abbreviations EPA, OA, AA and CO used in the sample records Experiment Overall Design: refer to the following : Experiment Overall Design: CO : AIN-76A (control) Experiment Overall Design: OA : AIN-76A (fat-free) + 1% corn oil + 3.7% oleic acid Experiment Overall Design: EPA : AIN-76A (fat-free) + 1% corn oil + 3.7% eicosapentaenoic acid Experiment Overall Design: AA : AIN-76A (fat-free) + 1% corn oil + 3.7% arachidonic acid Experiment Overall Design: Corn oil was supplemented with purified linoleic and alpha-linolenic acid to meet the nutritional requirements of mice for these essential fatty acids. Diets fed for 6 weeks.
2008-10-21 | E-GEOD-12028 | biostudies-arrayexpress
Project description:Blue mussel larvae were fed, in a first group, a balanced diet of essential fatty acids (EFAs) provided by a cocktail diet (COC) from three algal species. Larvae were cultured in three separate tanks from hatching, 0 day post-fertilization (DPF) until 42 DPF. Treated larvae were fed a deficient diet (Tiso) that contains low levels of arachidonic acid (AA) and eicosapentaenoic acid (EPA), two EFAs necessary for larval development, performance, and survival. The goal is to identify coordinated patterns of gene expression and understand their predictive function in relation to growth and mortality during early developmental stages of the blue mussel Mytilus edulis. In order to understand the mechanisms by which growth and survival drive an organism to the full range of its adaptation, we de novo assembled of the mussel transcriptome during early development using next-generation sequencing (NGS) technology, then designed customized microarrays targeting every developmental stage, which encompass major transitions in tissue organization of the fast-evolved blue mussel
2014-08-31 | GSE55580 | GEO
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)
2015-01-30 | E-GEOD-63254 | biostudies-arrayexpress
Project description:Elevated circulating lipid levels are known risk factors for cardiovascular diseases (CVD). In order to examine the effects of quercetin on hepatic lipid metabolism and detailed serum lipid profiles, mice received a mild-high-fat diet without (control) or with supplementation of 0.33% (w/w) quercetin for 12 weeks. Gas chromatography and 1H nuclear magnetic resonance were used to measure quantitatively serum lipid profiles and whole genome microarray analysis was used to identify the responsible mechanisms in liver. There were no significant differences found in mean body weight, energy intake and hepatic lipid accumulation between the quercetin and control group. In serum of quercetin-fed mice, TG levels were decreased with 15%, poly unsaturated fatty acids (PUFA) were increased with 14% and saturated fatty acids were decreased. Palmitic acid, oleic acid, and linoleic acid were all decreased in quercetin-fed mice by 9-15%. Both palmitic acid and oleic acid can be oxidized by omega-oxidation. Indeed, gene expression profiling showed that quercetin increased hepatic lipid metabolism, especially omega-oxidation. At the gene level, this was reflected by the up regulation of cytochrome P450 (Cyp) 4a10, Cyp4a14, Cyp4a31 and Acyl-CoA thioesterase 3 (Acot3). Two relevant regulators, Cytochrome P450 oxidoreductase (Por, rate limiting for cytochrome P450s) and the transcription factor Constitutive androstane receptor (Car; official symbol Nr1i3) were also up regulated in the quercetin-fed mice. We conclude that quercetin intake increased hepatic lipid omega-oxidation and lowered corresponding circulating lipid levels, a process that may involve Por and Car, and results in a potential beneficial CVD preventive effect. Liver samples were obtained from 36 C57BL/6J male adult mice. All mice started with a three week adaptation phase, in which they were fed a mild-high-fat diet. 12 mice were sacrificed immediately after the adaptation phase (t=0). The other 24 mice received the mild-high-fat diet without (HF) or with supplementation of 0.33% (w/w) quercetin (HF-Q) for 12 weeks.
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