Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA378597 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5331984.fastq.gz | Fastqsanger.gz | |||
| SRR5331969.fastq.gz | Fastqsanger.gz | |||
| SRR6930620.fastq.gz | Fastqsanger.gz | |||
| SRR6930630.fastq.gz | Fastqsanger.gz | |||
| SRR6930621.fastq.gz | Fastqsanger.gz |
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Project description:Transfer RNA-derived small RNAs (tsRNAs) are an emerging class of small RNAs, yet their regulatory roles have not been well understood. Here we studied the molecular mechanisms and consequences of tsRNA-mediated regulation in Drosophila. By carrying out mRNA sequencing and ribosome profiling of S2 cells transfected with single-stranded tsRNA mimics and mocks, we show that tsRNAs recognize target mRNAs through conserved complementary sequence matching and suppress target genes by translational inhibition. Serum starvation experiments confirm tsRNAs participate in cellular starvation responses by preferential targeting the ribosomal proteins and translational initiation or elongation factors. Knock-down of AGO2 in S2 cells under normal and starved conditions reveals a dependence of the tsRNA-mediated regulation on AGO2. Our study suggests the tsRNA-mediated regulation might be crucial for the energy homeostasis and the metabolic adaptation in the cellular systems.
2018-03-02 | GSE106697 | 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: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:Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a M-bM-^@M-^\low/low/high/lowM-bM-^@M-^] or M-bM-^@M-^\LLHLM-bM-^@M-^]. We found that mTORC1 regulated the expression of, among other lysosomal genes, V-ATPases through the transcription factor EB (TFEB, Tcfeb in the mouse). The knockdown of Tfeb resulted in the 'flattening' of the LLHL pattern and allowed the identification of genes regulated by mTORC1 through Tfeb Mouse embryo fibroblasts (MEFs) wild type or deficient in Tsc2 expressing a Tfeb shRNA or scrambled shRNA vector were treated with 25 nM rapamycin or vehicle (methanol) for 24 h under low serum conditions (0.1% FBS)
2011-08-02 | E-GEOD-28021 | biostudies-arrayexpress
Project description:Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a “low/low/high/low” or “LLHL”. We found that mTORC1 regulated the expression of, among other lysosomal genes, V-ATPases through the transcription factor EB (TFEB, Tcfeb in the mouse). The knockdown of Tfeb resulted in the 'flattening' of the LLHL pattern and allowed the identification of genes regulated by mTORC1 through Tfeb
2011-08-03 | GSE28021 | GEO
Project description:Objective Lung cancer has the highest incidence and mortality rates globally, with the majority of cases classified as non-small cell lung cancer (NSCLC). Due to the absence of specific tumor biomarkers, most lung cancer cases are diagnosed at an advanced stage. Therefore, the identification of novel molecular biomarkers with high sensitivity and specificity for early diagnosis is deemed crucial for enhancing the treatment of NSCLC. Transfer RNA-derived small RNA (tsRNA) is closely associated with malignant tumors and holds promise as a potential biomarker for tumor diagnosis. This study aimed to investigate whether serum tsRNA could serve as a biomarker for NSCLC. Methods Differentially expressed tsRNAs were identified through high-throughput sequencing of serum samples obtained from patients with NSCLC and healthy individuals. Additional serum samples were collected for validation using Reverse Transcription Quantitative Polymerase Chain Reaction (RT-qPCR). The diagnostic performance of these tsRNAs was assessed through Receiver Operating Characteristic (ROC) Curve Analysis. Furthermore, preliminary functional exploration was undertaken through cell experiments. Results tsRNA-49-73-Glu-CTC is highly expressed in the serum of patients with NSCLC and demonstrates superior diagnostic value compared to commonly used tumor markers in clinical practice, such as Carcinoembryonic Antigen (CEA), Neuron-Specific Enolase (NSE), and Cytokeratin 19 Fragment (CYFRA). A combined diagnostic approach enhances the accuracy of NSCLC detection. Additionally, tsRNA-49-73-Glu-CTC is highly expressed in A549 cells, and transfection with a tsRNA-49-73-Glu-CTC inhibitor significantly reduces both proliferation and migration capabilities. Conclusions tsRNA-49-73-Glu-CTC has the potential to serve as a novel molecular diagnostic biomarker for NSCLC and plays a significant role in the biological processes associated with NSCLC proliferation and migration.
2025-02-18 | GSE278659 | GEO
Project description:Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a M-^Slow/low/high/lowM-^T or M-^SLLHLM-^T, which allowed the identification of genes regulated by mTORC1 by performing the appropriate comparisons
2011-08-02 | E-GEOD-27982 | biostudies-arrayexpress