Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281415 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1979016_1.fastq.gz | Fastqsanger.gz | |||
| SRR1979016_2.fastq.gz | Fastqsanger.gz | |||
| SRR1979017_1.fastq.gz | Fastqsanger.gz | |||
| SRR1979017_2.fastq.gz | Fastqsanger.gz | |||
| SRR1979018_1.fastq.gz | Fastqsanger.gz |
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Project description:Leigh Syndrome (LS) is the most common early-onset, progressive mitochondrial encephalopathy usually leading to early death. The single most prevalent cause of LS is occurrence of mutations in the hSurf1 gene. LSSurf1 patients show a marked and specific decrease in the activity of mitochondrial respiratory chain complex IV (cytochrome c oxidase, COX). hSurf1 encodes an inner membrane mitochondrial protein involved in COX assembly. We established a D. melanogaster model of LS based on the post-transcriptional silencing of CG9943, the Drosophila homolog of hSurf1. Knock down of Surf1 was induced (i) ubiquitously, which led to larval lethality; (ii) in the mesodermal derivatives, which led to pupal lethality; (iii) in the central nervous system, which allowed survival; and (iv) at specific developmental stages. A biochemical characterization was carried out in knock down individuals, which unexpectedly revealed defects in all complexes of the mitochondrial respiratory chain (MRC) included the F-ATP synthase (complex V) in larvae, and a COX-specific impairment in adults. Silencing of Surf1 expression in Drosophila S2R+ cells led to loss of COX activity associated with decreased oxygen consumption. We conclude that Surf1 is essential for COX activity and mitochondrial function in D. melanogaster, and provide a new tool to clarify the pathogenic mechanisms of LS.
2014-11-04 | GSE58301 | GEO
Project description:Molecular alterations caused by mitochondrial alternative oxidase (AOX) expression in Drosophila melanogaster development
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Project description:Reversible and sub-lethal stresses to the mitochondria elicit a program of compensatory responses that ultimately improve mitochondrial function, a conserved anti-aging mechanism termed mitohormesis. Here, we show that harmol, a member of the beta-carbolines family with anti-depressant properties, improves mitochondrial function and metabolic parameters, and extends healthspan. Treatment with harmol induces a transient mitochondrial depolarization, a strong mitophagy response, and the AMPK compensatory pathway both in cultured C2C12 myotubes and in male mouse liver, brown adipose tissue and muscle, even though harmol crosses poorly the blood-brain barrier. Mechanistically, simultaneous modulation of the targets of harmol monoamine-oxidase B and GABA-A receptor reproduces harmol-induced mitochondrial improvements. Diet-induced pre-diabetic male mice improve their glucose tolerance, liver steatosis and insulin sensitivity after treatment with harmol. Harmol or a combination of monoamine oxidase B and GABA-A receptor modulators extend the lifespan of hermaphrodite Caenorhabditis elegans or female Drosophila melanogaster. Finally, two-year-old male and female mice treated with harmol exhibit delayed frailty onset with improved glycemia, exercise performance and strength. Our results reveal that peripheral targeting of monoamine oxidase B and GABA-A receptor, common antidepressant targets, extends healthspan through mitohormesis.
2023-05-26 | MTBLS7533 | MetaboLights
Project description:We used high throughput EST sequences to characterize and generate expression profiles for all transcripts encoded in the mitochondrial genome of D. melanogaster and D. pseudoobscura. Mapping of ESTs confirmed previously predicted transcripts and revealed non-canonical transcript structures. Expression of mitochondrial transcripts was not different between the two species, but it was significantly different for males and females. We also detected difference in expression levels among mRNAs from genes located in the same transcriptional unit and among genes interacting in the same protein complexes, NADH dehydrogenase and cytochrome c oxidase complexes, suggesting a complex post-transcriptional regulation to maintain mitochondrial function. Keywords: Transcriptome Analysis Four samples analysed: D. melanogaster males, D. melanogaster females, D. pseuoobscura males, D. pseudoobscura females The number of reads that mapped to each transcript is proportional to the transcript abundance, so it can be used as a measure of the absolute level of expression of that transcript. The gene expression measure as the absolute EST counts and the expression relative to the library size for each mitochondrial gene in each library is displayed in the supplementary file linked below.
2009-12-09 | E-GEOD-16651 | biostudies-arrayexpress
Project description:Comparative analysis of the transcriptional response, as quantified by RNA-Seq, of Mycobacterium tuberculosis (Mtb) during inhibition of the terminal cytochrome oxidases, Cytochrome bd oxidase and Cytochrome bcc:aa3. This study was designed to evaluate the efficacy if a novel small molecule inhibitor of the Cytochrome bd oxidase. Specifically, we compared the transcriptional response of Mtb during inhibition by Q203 with a Cytochrome bd deletion mutant to the transcriptional response of Mtb treated with a combination of Q203 and the purported Cytorchomre bd small molecule inhibitor (ND-011992).
2020-10-07 | GSE159080 | GEO
Project description:We used high throughput EST sequences to characterize and generate expression profiles for all transcripts encoded in the mitochondrial genome of D. melanogaster and D. pseudoobscura. Mapping of ESTs confirmed previously predicted transcripts and revealed non-canonical transcript structures. Expression of mitochondrial transcripts was not different between the two species, but it was significantly different for males and females. We also detected difference in expression levels among mRNAs from genes located in the same transcriptional unit and among genes interacting in the same protein complexes, NADH dehydrogenase and cytochrome c oxidase complexes, suggesting a complex post-transcriptional regulation to maintain mitochondrial function. Keywords: Transcriptome Analysis
2009-12-09 | GSE16651 | GEO
Project description:ITRAQ Phosphoproteomics revealed proteins associated with spermatogenesis in Wolbachia-Infected Male Drosophila Melanogaster
2024-09-29 | PXD026049 | Pride
Project description:MicroRNA microarray of Drosophila melanogaster extracted from cephalic complexes of lgl-hypomorph 3rd instar larvae
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Project description:Exposure to Paraquat and RNA interference knockdown of mitochondrial superoxide dismutase (Sod2) are known to result in significant lifespan reduction, locomotor dysfunction, and mitochondrial degeneration in Drosophila melanogaster. Both perturbations increase the flux of superoxide, a progenitor reactive oxygen species, but the molecular underpinnings of the resulting phenotypes are poorly understood. Improved understanding of such processes could lead to advances in the treatment of numerous age-related disorders. Superoxide toxicity can act through protein carbonylation. Analysis of carbonylated proteins is attractive since reactive carbonyl groups are not present in the twenty canonical amino acids and are amenable to labeling and enrichment strategies. Here, carbonylated proteins were labeled with biotin hydrazide and enriched on streptavidin-coated beads. On-bead digestion was used to release carbonylated protein peptides, with relative abundance ratios versus controls obtained using the iTRAQ mass spectrometry-based proteomics approach. While Paraquat exposure and Sod2 knockdown have similar phenotypes, differences in protein carbonylation were anticipated because Paraquat exposure was expected to increase the concentration of superoxide throughout the cell while Sod2 knockdown was only expected to raise the concentration of superoxide in the mitochondrial matrix. Paraquat exposure resulted in widespread increases in carbonylated protein relative abundance: the median Paraquat-exposed to control carbonylated protein relative abundance ratio was 1.53. For Sod2 knockdown, in contrast, the median carbonylated protein relative abundance ratios were 1.13 versus the RNA interference driver control and 1.05 versus the RNA interference transgene control. However, some proteins did show large increases in carbonylated protein relative abundance on Sod2 knockdown, most notably cytochrome c oxidase subunit Vb, possibly providing some indication of the molecular basis of the Sod2-knockdown phenotype.
2014-11-26 | PXD001528 | Pride
Project description:Spermiogenesis in Drosophila melanogaster is a highly conserved process and essential for male fertility. In this haploid phase of spermatogenesis, motile sperm are assembled from round cells, flagella are assembled, and needle-shaped nuclei with highly compacted genomes are formed. We aimed at identifying proteins relevant for the maturation phase from spermatids to sperm. As transcription takes place mainly in spermatocytes, and transcripts with relevance for post-meiotic sperm development are translationally repressed for days, we comparatively analysed the prote-ome of larval testes (stages before meiotic divisions), of testes of 1–2-day-old pupae (meiotic and early spermatid stages) and adult flies (late spermatids and sperm). We identified 6677 pro-teins, with 422 solely detected in larval testes, 623 in pupal testes and 634 in adult testes. We analysed a few so far uncharacterized proteins with repect to stage specific expression and im-portance for male fertility. For example, Mst84B (gene CG1988), a very basic cysteine- and lysine-rich nuclear protein, was present in the phase of transition from a histone-based to a pro-tamine-based chromatin structure. CG6332 encodes d-Theg, which is related to the mouse tHEG and human THEG proteins. Mutants of d-Theg lacked sperm in the seminal vesicles and were sterile. The identification of numerous predicted proteins underscores the high potential of pro-teome analysis for future analyses of spermatogenesis.
2019-02-01 | PXD010627 | Pride