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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [RNA-seq]

ABSTRACT: Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [RNA-seq]

PROVIDER: PRJNA1068076 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27698165_1.fastq.gz	Fastqsanger.gz
	SRR27698165_2.fastq.gz	Fastqsanger.gz
	SRR27698166_1.fastq.gz	Fastqsanger.gz
	SRR27698166_2.fastq.gz	Fastqsanger.gz
	SRR27698167_1.fastq.gz	Fastqsanger.gz

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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [Ribo-seq]

Project description:We show that Dhx9 deficiency restricts the development and homeostasis of enteric neuron, and specifically suppresses the early development of serotonergic neurons.

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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells

Project description:Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells

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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [Ribo-seq]

Project description:Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [Ribo-seq]

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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells [RNA-seq]

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Enteric neuronal GPR41-DHX9 signaling senses microbial metabolites to mediate the crosstalk between serotonergic neurons and intestinal stem cells

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

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Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9

Project description:The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach. Comparison of gene expression in large intestine of mice with or without reduced expression of DHX9.

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DHX9 and NPM1 silencing RNA-seq

Project description:In our study, we valided DHX9 and NPM1 interact with KIMAT1, whereas DHX9 also interacts with HIF1A-As2. DHX9 is a highly conserved DEAD-box protein expressed in the nucleus and the cytoplasm, involved in many processes including transcriptional activation, miRNA biogenesis and tumor cell maintenance. NPM1 is predominantly localized in the nucleoplasm, where it associates with active RNA polymerase II and transcriptionally activates genes involved in cancer. We silenced DHX9 and NPM1 and performed RNA-seq to examine the dysregulated genes by DHX9 and NPM1.

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Project description:Many traditional cytotoxic agents used in the treatment of cancer function by eliciting an apoptotic response in tumor cells. However, evasion of apoptosis by BCL-2 family members is often deregulated prior to therapeutic intervention leading to treatment failure. To address this, ABT-737 was rationally designed to target BCL-2-like family members and has shown promising results against tumor cells dependent on BCL-2 for their survival. One shortcoming is that MCL-1, a member of the BCL-2 family is poorly inhibited by ABT-737 and is a major cause of resistance. To gain insight into biological pathways that could circumvent this resistance, we designed an shRNA screen to identify novel sensitizers to ABT-737 by engineering MYC driven lymphomas that were resistant to ABT-737 due to endogenous MCL-1 expression. Utilizing this model, we performed a shRNA drop-out screen and identified Dhx9 as a target whose suppression sensitizes cells to ABT-737. DHX9 loss lead to replicative stress signaling, which in turn potently induced the BH3-only proteins, NOXA and PUMA, in a p53-dependent manner to curtail MCL-1 activity. Induction of NOXA is essential for ABT-737 sensitization. Our results ascribe a novel role for DHX9 in the replicative stress pathway and link DHX9 activity to p53 function in vivo. Comparison of Arf-/-Eu-myc/Bcl-2 lymphomas expressing either control Rluc.713 or Dhx9 shRNA, Dhx9.1241

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