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ABSTRACT:
PROVIDER: PRJNA238901 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim was to identify genes whose transcription is induced or repressed by REPTOR (=CG13624) KO in Drosophila melanogaster male adults. Data are part of the manuscript REPTOR and REPTOR-BP regulate organismal metabolism and transcription downstream of mTORC1 2 biological replicates from 2 conditions: Control adult males / REPTOR KO adult males ; 4 samples
2015-04-30 | E-GEOD-64846 | biostudies-arrayexpress
Project description:The aim was to identify genes whose transcription is induced or repressed by REPTOR (=CG13624) KO in Drosophila melanogaster male adults. Data are part of the manuscript REPTOR and REPTOR-BP regulate organismal metabolism and transcription downstream of mTORC1
2015-04-30 | GSE64846 | GEO
Project description:The first aim was to identify genes whose transcription is induced by rapamycin feeding in Drosophila S2 cells. Secondly, the goal was to find out which contribution the transcription factors REPTOR (=CG13624) and REPTOR-BP (REPTOR-binding partner, =CG18619) has to the observed changes in expression. We thus compared gene epxression between rapamycin and control treated S2 cells in GFP, REPTOR or REPTOR-BP knockdown cells.
2015-04-30 | GSE55219 | GEO
Project description:The first aim was to identify genes whose transcription is induced by rapamycin feeding in Drosophila S2 cells. Secondly, the goal was to find out which contribution the transcription factors REPTOR (=CG13624) and REPTOR-BP (REPTOR-binding partner, =CG18619) has to the observed changes in expression. We thus compared gene epxression between rapamycin and control treated S2 cells in GFP, REPTOR or REPTOR-BP knockdown cells. 3 biological replicates from control knockdown plus/minus rapamycin and REPTOR knockdown plus/minus rapamycin; 2 biological replicates from REPTOR-BP knockdown cells plus/minus rapamycin; together those are 16 samples
2015-04-30 | E-GEOD-55219 | biostudies-arrayexpress
Project description:Purpose: REPTOR and FoxO are two transcription factors that regulate muscle metabolism. However, these transcription factors share around 40% of target genes. Furthermore, the thorax of adult flies is composed of several tissues including muscle and fat body, making it difficult to discover direct target genes of REPTOR and FoxO specifically in muscle tissue. This experimental approach allows the identification of REPTOR-specific and FoxO-specific target genes in muscle clusters Methods: snRNA-seq analysis of dissected adult fly thoraces, when an active allele of REPTOR or an active allele of FoxO are overexpressed using a muscle-specific driver (dMef2-Gal4) Results: Identification of the transcriptional signature of each tissue present in the thorax of adult flies when REPTOR or FoxO are overexpressed in muscle. Discovery of potential direct target genes of REPTOR and FoxO in muscle tissue, as well as metabolic pathways regulated by each transcription factor. Conclusions: REPTOR and FoxO modulate distinct gene signatures in muscle tissue to regulate metabolism in adult flies.
2023-06-01 | GSE227038 | GEO
Project description:Mechanistic target of rapamycin complex 1 (mTORC1) senses amino acid availability to orchestrate metabolic processes critical for physiological homeostasis and organismal ageing 1. While mTORC1 preferentially regulates the translation of 5′-terminal oligopyrimidine (TOP) motif-containing mRNAs that predominantly encode ribosomal proteins (RPs) via the translational repressor 4E-BP 2, this mTORC1 function is resistant to rapamycin inhibition 3. TOP mRNAs are exceptionally abundant, thus imposing a major translational burden on cells; yet how their translation is physiologically tuned and linked to longevity remain unexplored. Here we identify Lsp2, originally known as a storage protein 4, as an adipose effector of mTORC1 that modulates lifespan in Drosophila. Lsp2 is induced by essential amino acids (EAAs) via mTORC1. Genetic ablation of Lsp2 to blunt organismal response to protein diets drives robust lifespan extension without compromising key life-history traits such as reproduction. Translatomic profiling reveals that loss of Lsp2 selectively reduces global TOP mRNA translation in a 4E-BP-dependent manner, thereby extending lifespan via a mechanism distinct from rapamycin inhibition. Finally, Lsp2 adipokine promotes 4E-BP phosphorylation and acts systemically across tissues to shape the lifespan responses to dietary protein. Collectively, our findings establish Lsp2 as a novel translational regulator of TOP genes that mechanistically couples physiological ribosomal protein synthesis with organismal longevity.
2026-07-15 | GSE297586 | GEO
Project description:Purpose: identify global changes in gene expression in thorax tissues caused by an increase in activity of REPTOR in muscles. Note that the thorax of adult flies is composed mainly by muscle tissue but fat body is also present. Changes in gene expression do not exclusively reflect the muscle transcriptome Methods: To extract total RNAs for RNA-Seq experiment, we used 5-6 thoraces dissected out from both tub-Gal80ts/+ ; dMef2-GAL4/+ (Con) and tub-Gal80ts/UAS-REPTOR[ACT] ; dMef2-GAL4/+ (REPTOR), making sure the gut of these flies was completely removed. Crosses were kept at 18°C to avoid expression of REPTOR during development. Adult males were collected every 24-48 hours and incubated 3-4 days at 18°C before being shifted to 29°C. Flies were then incubated for 4 days at 29°C. After assessing RNA quality with Agilent Bioanalyzer, mRNAs were enriched by poly-A pull-down. Then, sequencing libraries constructed with Illumina TruSeq RNA prep kit were sequenced using. We multiplexed samples in each lane, which yields targeted number of single-end 75 bp reads for each sample, as a fraction of 180 million reads for the whole lane. Sequence reads were mapped back to the Drosophila genome (flybase genome annotation version r6.30) using STAR. With the uniquely mapped reads, we quantified gene expression levels using Cufflinks (FPKM values). Next, differentially expressed genes between experimental and control data were analyzed with DESeq2. Results: Gene list enrichment analysis of the downregulated thoracic transcriptome by REPTOR overexpression revealed a striking enrichment of multiple metabolic processes impinging on carbohydrate metabolism, mitochondria, glycolysis and oxidative metabolism. Also, Thor, a well-characterized target of REPTOR was upregulated and it was validated with qPCR. Conclusions: Our study indicates that REPTOR is a strong regulator of muscle metabolism in adult flies.
2023-06-01 | GSE189218 | GEO
Project description:Gene expression after rapamycin treatment in control, REPTOR or REPTOR-BP knockdown S2 cells
| PRJNA238905 | ENA
Project description:Mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway is activated by nutrition sufficiency signals and extracellular growth signals. mTORC1 acts the hub that integrates these inputs to orchestrate number of cellular responses such as translation, nucleotide synthesis, lipid synthesis, and lysosome biogenesis. However, the scaffold protein which specifically regulates any single downstream signaling molecule has not been identified to date. Here we show the heteropentamer protein complex Ragulator is critically required to regulate nuclear translocation of transcription factor EB (TFEB). We established a unique RAW264.7 clone that lacks Ragulator but maintained total mTORC1 activity. The clone showed a markedly enhanced nuclear translocation of TFEB even in nutrition-sufficient state, despite the full mTORC1 activity. As a cellular phenotype, the number of lysosomes were increased by 10 times in the Ragulator-deficient clone. These findings suggest that mTORC1 essentially requires the scaffold Ragulator to regulate the subcellular location of TFEB. Our finding implicates that mTORC1 has other scaffold proteins that regulate downstream molecules specifically.
2021-08-08 | GSE171357 | GEO
Project description:mTOR complex 1 (mTORC1) senses nutrient availability and instructs accordingly fundamental metabolic processes including protein synthesis to maintain physiological homeostasis. Reducing mTORC1 activity by caloric restriction, rapamycin treatment, or genetic manipulation, extends lifespan in diverse model organisms, yet how to rationally design strategies for mTORC1 intervention without compromising normal organismal physiology remains to be explored. Using Drosophila model, we report here the characterization of an adipokine, Lsp2, as a nutrient-dependent regulator of mTORC1 signaling outputs. This adipokine is strongly induced by protein diets and controlled by the insulin-mTORC1 signaling axis, while reminiscent of their effects in ageing, Lsp2 negatively regulates lifespan. Loss of Lsp2 robustly extends lifespan and health span notably on protein-rich diets by specifically and globally reducing 4E-BP-dependent translation of ribosomal proteins, a mechanism distinct from that of rapamycin. Our data thus support a novel concept that an inducible mechanism that enhances the translation of proteins making up the translation machinery, is encoded beyond the mTORC1-4E-BP core signaling module, and targeting such auxiliary translation-enhancing mechanism provides health benefits in the context of ageing and overnutrition.
2026-07-16 | GSE295794 | GEO