Ontology highlight
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:Mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient availability to orchestrate metabolic processes critical for physiological homeostasis and organismal aging. 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, this mTORC1 function is resistant to rapamycin inhibition. 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, as an adipose effector and feedback activator of mTORC1 that modulates lifespan in Drosophila. Lsp2 expression is induced by essential amino acids (EAAs) via mTORC1 and gated by additional signals of nutrient sufficiency. Genetic ablation of Lsp2 robustly extends lifespan without impairing key life-history traits such as reproduction. Translatomic profiling shows 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. Evolutionarily, TOP motifs co-emerged with 4E-BP and are present in nearly all Drosophila RP mRNAs. Moreover, we demonstrate that their role in translational control extends to Drosophila. Collectively, our findings reveal a nutrient-induced physiological factor that amplifies mTORC1 output in TOP mRNA translation and regulates organismal longevity.
| PXD063648 |
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:Mechanistic target of rapamycin complex 1 (mTORC1) senses nutrient availability to orchestrate metabolic processes critical for physiological homeostasis and organismal aging 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 and feedback activator of mTORC1 that modulates lifespan in Drosophila. Lsp2 expression is induced by essential amino acids (EAAs) via mTORC1 and gated by additional signals of nutrient sufficiency. Genetic ablation of Lsp2 robustly extends lifespan without impairing key life-history traits such as reproduction. Translatomic profiling shows 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. Evolutionarily, TOP motifs co-emerged with 4E-BP and are present in nearly all Drosophila RP mRNAs. Moreover, we demonstrate that their role in translational control extends to Drosophila. Collectively, our findings reveal a nutrient-induced physiological factor that amplifies mTORC1 output in TOP mRNA translation and regulates organismal longevity.
2026-07-16 | GSE295794 | GEO
Project description:Gene expression after rapamycin treatment in control, REPTOR or REPTOR-BP knockdown S2 cells
| PRJNA238905 | ENA