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YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [MCF10A]

ABSTRACT: YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [MCF10A]

PROVIDER: PRJNA930428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23304986_1.fastq.gz	Fastqsanger.gz
	SRR23304986_2.fastq.gz	Fastqsanger.gz
	SRR23304987_1.fastq.gz	Fastqsanger.gz
	SRR23304987_2.fastq.gz	Fastqsanger.gz
	SRR23304988_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [MCF10A]

Project description:The Hippo pathway downstream effectors YAP and TAZ display oncogenic potential via their transcriptional co-activator function, mediated primarily by binding to TEAD transcription factors. Many studies have focused on identifying YAP/TAZ-TEAD target genes, but their role in the regulation of protein synthesis has remained largely unexplored. Here we show that YAP activation is sufficient to overcome the global translation restriction of 5TOP-containing mRNAs, which is induced by serum deprivation and dependent on the inactivation of mTORC1. We found that YAP/TAZ repressed the expression of DDIT4, a negative regulator of mTORC1 whose expression is otherwise upregulated by serum deprivation. Forced expression of DDIT4 was sufficient to suppress translation and transformative potential of serum-unresponsive uveal melanoma cells, which harbor G protein mutations. Our findings highlight crosstalk between Hippo-YAP/TAZ and mTORC1 pathways in the regulation of translation and offer a new perspective towards understanding YAP/TAZ-driven malignancies.

2024-10-01 | GSE224260 | GEO

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [293AD]

2024-10-01 | GSE224261 | GEO

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [Ribo-seq]

2024-10-01 | GSE224263 | GEO

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity

Project description:YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity

| PRJNA930423 | ENA

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [293AD]

Project description:YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [293AD]

| PRJNA930427 | ENA

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [Ribo-seq]

Project description:YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity [Ribo-seq]

| PRJNA930426 | ENA

YAP overcomes restriction of translation induced by nutrient deprivation through restoration of mTORC1 activity

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-10-01 | GSE224264 | GEO

Nutrient deprivation elicits a transcriptional and translational inflammatory response coupled to decreased protein synthesis

Project description:Purpose: The goal of this study is to examine gene expression regulation at the transcriptional and translational levels in response to various forms of nutrient deprivation, and whether there are differences between isogenic transformed and non-transformed cells. Mehods: We apply high-throughput sequencing of ribosome footprints (ribosome profiling) and poly(A) RNA (RNA sequencing) in an isogenic pair of transformed (tamoxifen-treated) and non-transformed (ethanol control) MCF10A-ER-Src cells subjected to the metabolic stresses that differentially affect global protein synthesis (Figure 1): deprivation of glutamine (for 30min and 4 hours), glucose (4hours), cysteine/cystine (4hours) or leucine/isoleucine/valine (brach-chain aminoacids - BCAA) (4hours). The same experiments were also performed in transformed ER-Src MCF10A treated with torin1 (500nM) for 4 hours. Results: Genome-wide translational profiling of glutamine deprived ER-Src MCF10A cells (for 30 minutes) shows increased translation of uORFs-containing mRNAs and down-regulation of ribosomal protein mRNAs, which is followed by increased translation and transcription of cytokine and inflammatory mRNAs (after 4 hours of glutamine deprivation). The transcription and translation of inflammatory and cytokine mRNAs is also stimulated in response to 4 hours deprivation of glucose, cysteine/cystine and BCAA, with the extent of stimulation correlating with the i) decrease in global protein synthesis and ii) down-regulation of all translationally-repressed mRNAs or ribosomal protein mRNAs. Conclusions: Pro-inflammatory gene expression is associated with translational repression in response to short-term nutrient deprivation.

2018-07-01 | GSE114794 | GEO

A bi-steric mTORC1-selective inhibitor overcomes drug resistance in breast cancer

Project description:A bi-steric mTORC1-selective inhibitor overcomes drug resistance in breast cancer

| PRJNA962031 | ENA

Transcription profiling by array of mouse immortalized embryonic fibroblasts to identify genes regulated by mTORC1

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

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