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

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

PROVIDER: PRJNA930423 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23305229_1.fastq.gz	Fastqsanger.gz
	SRR23305229_2.fastq.gz	Fastqsanger.gz
	SRR23305230_1.fastq.gz	Fastqsanger.gz
	SRR23305230_2.fastq.gz	Fastqsanger.gz
	SRR23305131.fastq.gz	Fastqsanger.gz

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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]

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

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

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

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 | GSE224261 | GEO

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

2024-10-01 | GSE224260 | GEO

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 [Ribo-seq]

2024-10-01 | GSE224263 | GEO

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

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

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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

Identification of Tfeb-dependent genes downstream of mTORC1 in MEFs

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

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