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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus

ABSTRACT: TFEB and TFE3 are required for efficient cellular response against beta-coronavirus

PROVIDER: PRJNA867005 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20946807_1.fastq.gz	Fastqsanger.gz
	SRR20946807_2.fastq.gz	Fastqsanger.gz
	SRR20946808_1.fastq.gz	Fastqsanger.gz
	SRR20946808_2.fastq.gz	Fastqsanger.gz
	SRR20946809_1.fastq.gz	Fastqsanger.gz

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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [ChIP-Seq]

Project description:The transcription factors EB and E3 (TFEB and TFE3) promote lysosomal biogenesis and autophagy in response to a variety of stress conditions. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) belongs to the ß-coronaviruses family. Recent studies have shown that ß-coronaviruses use lysosomes to egress the cell. The aim of this work is to analyze if ß-coronavirus infection promotes TFEB/3 activation and to evaluate the contribution of these transcription factors to the cellular response upon viral infection.

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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [RNA-seq]

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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [RNA-seq]

Project description:TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [RNA-seq]

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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [ChIP-Seq]

Project description:TFEB and TFE3 are required for efficient cellular response against beta-coronavirus [ChIP-Seq]

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TFEB AND TFE3 DRIVE KIDNEY CYSTOGENESIS AND TUMORIGENESIS

Project description:Birt-Hogg-Dubè (BHD) syndrome is an inherited condition caused by loss-of-function mutations in the gene encoding the tumor-suppressor protein folliculin (FLCN) and frequently associated with kidney cysts and cancer. FLCN acts as a negative regulator of TFEB and TFE3 transcription factors, master controllers of lysosomal biogenesis and autophagy, by enabling their phosphorylation by the mechanistic Target Of Rapamycin Complex 1 (mTORC1). We previously showed that deletion of TFEB rescued the renal cystic phenotype of kidney-specific Flcn KO mice. Using Flcn/TFEB/TFE3 double and triple KO mice we now show that both TFEB and TFE3 contribute, in a differential and cooperative manner, to kidney cystogenesis. Importantly, silencing of either TFEB or TFE3 rescued tumorigenesis in patient-derived xenografts (PDXs) generated from a kidney tumor of a BHD patient. Furthermore, transcriptome analyses performed in transgenic mice, PDXs and patient tumor samples revealed TFEB/TFE3 downstream targets that may contribute to their tumorigenic activity. Our findings demonstrate in disease-relevant models that TFEB and TFE3 are key drivers of kidney tumorigenesis and suggest novel therapeutic strategies based on the inhibition of these transcription factors.

2023-04-04 | PXD035450 | Pride

Transcriptional regulation of the innate immune reponse by the MITF/TFE3 family

Project description:To understand the activation of the MITF/TFE transcription factors in effective defense against pathogens we examined the genome wide distribution of TFE3 in control and activated mouse macrophages. It was determined that TFEB and TFE3 collaborate with each other to promote efficient autophagy induction, increased lysosomal biogenesis, and transcriptional upregulation of proinflammatory cytokines and key mediators of the inflammatory response. 4 samples were analyzed: Background Control, Control, Starvation, LPS

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TFEB and TFE3 are required for efficient cellular response against beta-coronavirus

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

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The FACT complex facilitates expression of lysosomal and antioxidant genes through binding to TFEB and TFE3 [RNA-seq]

Project description:The transcription factors TFEB and TFE3 orchestrate the cellular response to a variety of stressors, including nutrient deprivation, oxidative stress, and pathogens. Here we describe a novel interaction between TFEB/TFE3 and FACT, a heterodimeric histone chaperone consisting of SSRP1 and SPT16 that mediates nucleosome disassembly and assembly, thus facilitating transcription. Extracellular stimuli, such as nutrient deprivation or oxidative stress, induce nuclear translocation and activation of TFEB and TFE3, which then associate with the FACT complex to regulate stress-induced gene transcription. Depletion of FACT does not affect TFEB activation, stability, or binding to the promoter of target genes. In contrast, reduction of FACT levels by siRNA or treatment with the FACT inhibitor curaxin, severely impair induction of numerous antioxidant and lysosomal genes, revealing a crucial role of FACT as a regulator of cellular homeostasis. Furthermore, upregulation of antioxidant genes induced by TFEB over-expression is significantly reduced by curaxin, consistent with a role of FACT as a TFEB transcriptional activator. Together, our data show that chromatin remodeling at the promoter of stress-responsive genes by FACT is important for efficient expression of TFEB/TFE3 targets, thus providing a link between environmental changes, chromatin modifications and transcriptional regulation.

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The FACT complex facilitates expression of lysosomal and antioxidant genes through binding to TFEB and TFE3 [ChIP-seq]

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2023-07-31 | GSE155220 | GEO

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