Drosophila melanogaster
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-25007
PROVIDER: PRJNA142725 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:gene expression profiles in fly brains between wildtype and miR-34 null flies gene expression profiles in fly brains, wild type (3d, 20d) and miR-34 null flies (3d, 20d)
2011-12-23 | E-GEOD-25008 | biostudies-arrayexpress
Project description:gene expression profiles in fly brains between wildtype and miR-34 null flies
2011-12-23 | GSE25008 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE24992: Drosophila brain microRNA expression with age: miRNA profiling GSE25007: Drosophila brain gene expression with age: mRNA profiling GSE25008: Drosophila brain gene expression between wildtype and miR-34 null flies Refer to individual Series. Aging is the most prominent risk factor for human neurodegenerative disease, but underlying mechanisms that connect two processes are less well characterized. With age, the brain undergoes functional decline and perhaps degeneration. Such decline may not just contribute to normal aging, but also enhance susceptibility to and progression of age-related neurodegenerative diseases. Therefore, defining intrinsic factors and pathways that underline the normal integrity of the adult nervous system may lead to insights that potentially link aging and neurodegeneration. Here, we report a highly conserved microRNA (miRNA), miR-34, as a modulator of aging and neurodegeneration. Using Drosophila, we show that fly miR-34 expression is brain-enriched and strikingly upregulated with age. Functional studies reveal that, whereas animals without miR-34 are normal as young adults, upon aging, they gradually show late-onset deficits characteristic of accelerated brain aging; these include a transcriptional signature of aged animals, coupled with rapid functional decline, loss of brain integrity, followed by a catastrophic decline in adult viability. Moreover, upregulation of miR-34 protects against neurodegeneration induced by pathogenic human polyglutamine (polyQ) disease protein. We next reveal a dramatic effect of miR-34 to silence the Eip74EF gene of steroid hormone pathways in the adult, which is crucial to maintain the normal aging. Collectively, these data define a miR-34-mediated mechanism that specifically affects long-term integrity of the adult nervous system. miR-34 function in Drosophila may thus present a link that functionally connects aging and neurodegeneration. Our studies implicate essential roles of miRNA- dependent pathways in maintenance of the adult brain, disease pathogenesis and healthy aging.
2011-12-23 | E-GEOD-25009 | biostudies-arrayexpress
Project description:Chronic high-sugar feeding (1 M or 34% sucrose) leads to hyperglycemia, obesity, and insulin resistance in adult flies, compared with those fed a control diet (0.15 M or 5% sucrose). We compared two days and four weeks of high-sugar feeding to look at short- and long- term effects on gene expression. We used Affymetrix Drosophila GeneChip 2.0 microarrays to quantify differential expression between control and high-sugar-fed flies at two time points.
2017-10-21 | GSE105448 | GEO
Project description:dFOXO targets in adult Drosophila melanogaster females, and the effect of insulin signalling and stress on binding. The experimets determined the binding locations of dFOXO in the whole adult female fly using ChIP-chip. The protocol was validated using mock conditions: pre-immune serum or IP on chromatin from foxo null flies. The response of this binding to stress induced by treatment of flies with paraquat or by their exposure to starvation, as well as the response to an insulin-signalling-reducing genetic manipulation (over-expression of dominant negative form of the insulin receptor), was determined.
2011-06-18 | E-TABM-751 | biostudies-arrayexpress
Project description:<p>Chronic sleep loss profoundly impacts metabolic health and shortens lifespan, but studies of the mechanisms involved have focused largely on acute sleep deprivation. To identify metabolic consequences of chronically reduced sleep, we conducted unbiased metabolomics on heads of three adult Drosophila short-sleeping mutants with very different mechanisms of sleep loss: fumin (fmn), redeye (rye), and sleepless (sss). Common features included elevated ornithine and polyamines, with lipid, acyl-carnitine, and TCA cycle changes suggesting mitochondrial dysfunction. Studies of excretion demonstrate inefficient nitrogen elimination in adult sleep mutants, likely contributing to their polyamine accumulation. Increasing levels of polyamines, particularly putrescine, promote sleep in control flies but poison sleep mutants. This parallels the broadly enhanced toxicity of high dietary nitrogen load from protein in chronically sleep-restricted Drosophila, including both sleep mutants and flies with hyper-activated wake-promoting neurons. Together, our results implicate nitrogen stress as a novel mechanism linking chronic sleep loss to adverse health outcomes-and perhaps for linking food and sleep homeostasis at the cellular level in healthy organisms.</p>
2023-03-18 | MTBLS3318 | MetaboLights
Project description:Aging is a risk factor for neurodegenerative disease, but precise mechanisms that influence this relationship are still under investigation. Work in Drosophila melanogaster identified the microRNA miR-34 as a modifier of aging and neurodegeneration in the brain. MiR-34 mutants present aspects of early aging, including reduced lifespan, neurodegeneration, and a buildup of the repressive histone mark H3K27me3. To better understand how miR-34 regulated pathways contribute to age-associated phenotypes in the brain, here we transcriptionally profiled the miR-34 mutant brain. This identified that genes associated with translation are dysregulated in the miR-34 mutant. The brains of these animals show increased translation activity, accumulation of protein aggregation markers, and altered autophagy activity. To determine if altered H3K27me3 was responsible for this proteostasis dysregulation, we studied the effects of increased H3K27me3 by mutating the histone demethylase Utx. Reduced Utx activity enhanced neurodegeneration and mimicked the protein accumulation seen in miR-34 mutant brains. However, unlike the miR-34 mutant, Utx mutant brains did not show similar altered autophagy or translation activity, suggesting that additional miR-34-targeted pathways are involved. Transcriptional analysis of predicted miR-34 targets identified Lst8, a subunit of Tor Complex 1 (TORC1), as a potential target. We confirmed that miR-34 regulates the 3’ UTR of Lst8. Biological analysis of miR-34 mutant brains demonstrate that 4E-BP is hyperphosphorylated, consistent with increased Lst8 activity and changes in translation. Together, these results present novel understanding of brain aging and the role of the conserved miRNA miR-34 in impacting proteostasis in the brain with age.
2022-03-16 | GSE184559 | GEO
Project description:mRNA microarray of Drosophila wing imaginal discs or brain complexes from lgl27S3/lglE2S31 (lgl-null), scrib1/scrib2 or wild-type 3rd instar larvae RNA was isolated from 20 pairs of wing discs/brain complexes per sample (i.e 20 individuals). Samples were from 5 day AED wildtype and 9 day AED mutant tissue
2014-01-31 | GSE48852 | GEO
Project description:Aging is a prominent risk factor for neurodegenerative disease, therefore defining mechanisms critical for healthy brain aging should lead to insight into genes that modulate susceptibility to disease. To define such genes, we have pursued analysis of miR-34 mutants in Drosophila. The miR-34 mutant brain displays a gene profile of accelerated aging, and miR-34 upregulation is a potent suppressor of polyglutamine-induced neurodegeneration. We investigated targets of miR-34 to define those important for its functions in mitigating degeneration and impacting health of the brain with age. These studies show that miR-34 targets for silencing two components of polycomb repressive complex 2 (PRC2)—Pcl and Su(z)12—in the brain with age. PRC2 is a histone methyltransferase that confers the repressive H3K27me3 mark, suggesting that a critical role of miR-34 is to modulate the function of PRC2 to silence key genes in the brain with age. Remarkably, gene expression profiling of the brains of hypomorphic mutants in Enhancer of zeste (E(z)), the enzymatic methyltransferase component of PRC2, revealed a younger brain transcriptome profile and identified the small heat shock proteins as key modulated genes. These findings indicate that PRC2 epigenetic mechanisms impact the susceptibility of the brain to degenerative disease with age, and highlight the role of small heat shock proteins to protect the brain from age-associated decline and disease.
2018-10-10 | GSE110135 | GEO
Project description:Expression data from testes of CG3875 knockout and wildtype flies
| PRJNA127401 | ENA