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Gene expression profile of UOK257 cells silenced for TFEB or TFE3 relative to control UOK257 silenced for luciferase

ABSTRACT: Gene expression profile of UOK257 cells silenced for TFEB or TFE3 relative to control UOK257 silenced for luciferase

PROVIDER: PRJNA856616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20017589.fastq.gz	Fastqsanger.gz
	SRR20017590.fastq.gz	Fastqsanger.gz
	SRR20017591.fastq.gz	Fastqsanger.gz
	SRR20017592.fastq.gz	Fastqsanger.gz
	SRR20017593.fastq.gz	Fastqsanger.gz

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Gene expression profile of UOK257 cells silenced for TFEB or TFE3 relative to control UOK257 silenced for luciferase

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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.

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TFEB and TFE3 regulate STING1-dependent immune responses by controlling type I interferon signaling

Project description:STING1 is an essential component of the innate immune defense against a wide variety of pathogens. Whereas induction of Type I interferon (IFN) responses is one of the best-defined functions of STING1, our transcriptomic analysis revealed IFN-independent activities of STING1 in macrophages, including transcriptional upregulation of numerous lysosomal and autophagic genes. This upregulation was mediated by the STING1-induced activation of the transcription factors TFEB and TFE3, and led to increased autophagy, lysosomal biogenesis, and lysosomal acidification. TFEB and TFE3 also modulated IFN-dependent STING1 signaling by controlling IRF3 activation. IFN production and cell death were increased in TFEB and TFE3 depleted iBMDMs. Conversely, TFEB over-expression led to reduced IRF3 activation and an almost complete inhibition of interferon synthesis and secretion, resulting in decrease caspase-3 activation and increased cell survival. Our study reveals a key role of TFEB and TFE3 as regulators of STING1-mediated innate antiviral immunity.

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TFEB and TFE3 regulate STING1-dependent immune responses by controlling type I interferon signaling [AM_NIH_RNASeq_50538]

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TFEB and TFE3 regulate STING1-dependent immune responses by controlling type I interferon signaling [Q48645_RNAseq]

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Project description:Lysosomal degradation of the endoplasmic reticulum (ER) via autophagy (ER-phagy) is emerging as a critical regulator of cell homeostasis and function1. The recent identification of ER-phagy receptors has shed light on the molecular mechanism underlining this process; however, the signaling pathways regulating ER-phagy in response to cellular needs are still largely unknown. We found that the nutrient responsive transcription factors TFEB and TFE3 - master regulators of lysosomal biogenesis and autophagy2- control ER-phagy by inducing the expression of the ER-phagy receptor FAM134B. The TFEB/TFE3-FAM134B axis promotes ER-phagy activation upon prolonged starvation. In addition, we discovered that this pathway is activated in chondrocytes by FGF signaling, a critical regulator of cell differentiation 3. FGF signaling induces a JNK-dependent proteasomal degradation of the insulin receptor substrate 1, which inhibits the insulin-PI3K-PKB/Akt-mTORC1 pathway and promotes TFEB/TFE3 nuclear translocation and FAM134B induction. Consistent with a role of the TFEB/TFE3-FAM134B axis in chondrocytes, FAM134B knock-down impairs cartilage growth and mineralization in medaka fish. This study identifies a new signaling pathway that allows ER-phagy to respond to both metabolic and developmental cues.

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Transcriptome analysis of control and TFEB/TFE3 DKO RAW264.7 in response to DNA Damage

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Transcriptome analysis of control and TFEB/TFE3 DKO MEFs in response to DNA Damage

Project description:We analyze the contribution of the transcription fators TFEB and TFE3 to the DNA Damage Response (DDR)

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