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Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

ABSTRACT: Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

PROVIDER: PRJNA489601 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7792200.fastq.gz	Fastqsanger.gz
	SRR7792195.fastq.gz	Fastqsanger.gz
	SRR7792196.fastq.gz	Fastqsanger.gz
	SRR7792197.fastq.gz	Fastqsanger.gz
	SRR7792198.fastq.gz	Fastqsanger.gz

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Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

Project description:Metabolic programs and host defense are highly integrated to ensure proper immune responses during stress. Central to these responses, mTOR regulates immune functions by sensing and integrating environmental cues, yet how these systems are coordinated at the intestinal surface remains undefined. We show that the antimicrobial peptide α-defensin is functionally sustained during nutrient deprivation due to regulation of defensin-processing enzyme MMP7 by microbiota- and host-derived factors. Unlike other antimicrobial peptides, the MMP7-α-defensin axis remains active during nutrient fluctuations, providing essential protection against enteric pathogens. Sustained Mmp7 expression requires the microbiota and is mediated by de-repression of the transcription activator Atoh1 upon attenuation of the transcriptional repressor Hes1 in intestinal epithelial cells. Hes1 levels are regulated via mTOR and controlled translationally, constituting a metabolism-translation-transcription loop. Disrupting this loop by supplying nutrients paradoxically compromises anti-bacterial defense. Together, these results uncover a regulatory circuit that couples host nutrient status to epithelial anti-microbial immunity.

2019-03-25 | GSE119568 | GEO

Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

Project description:To investigate whether intestinal Hes1 expression was translationally regulated during nutrient deprivation, we performed ribosome profiling of ileum from fed and fasted mice.

2019-03-25 | GSE119567 | GEO

Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

Project description:Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

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Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

Project description:Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

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Nutrient sensing by the intestinal epithelium orchestrates mucosal antimicrobial defense via translational control of Hes1

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

2019-03-25 | GSE119569 | GEO

Gene expression alteration in chondrocyte by HES1 overexpression

Project description:To investigate target molecules of HES1, we transduced GFP or HES1 into mouse chondrocyte cell line ATDC5, and performed the microarray analysis. HES1 overexpression increased inflammation-related genes including Il6 and Il1rl1.

2015-03-02 | GSE60737 | GEO

Hes1 and Liver Glucocorticoid Signaling

Project description:To investigate the role of HES1 during glucocorticoid signaling in the liver, we employed whole-genome microarray expressions in liver mRNA extracted from control and Hes1-liver knockout male mice (HESKOL) that had been adrenalectomized to remove endogenous glucocorticoids.

2014-01-08 | GSE52106 | GEO

Decoding the DNA binding sites associated with HES1

Project description:To investigate the DNA binding sites associated with HES1, a CUT & Tag assay was conducted utilizing an anti-flag antibody to isolate the DNA sequences that interact with HES1. Subsequently, these DNA sequences were subjected to analysis through DNA-seq. The results indicated that HES1 has the capability to bind to the promotor-transcription start sites of 1140 genes.

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Expression analysis of common myeloid progenitors (CMPs) expressing Hes1

Project description:High levels of Hes1 expression are frequently found in BCR-ABL-positive chronic myelogenous leukemia in blast crisis (CML-BC). In mouse bone marrow transplantation (BMT) models, co-expression of BCR-ABL and Hes1 induces CML-BC–like disease; however the underlying mechanism remained elusive. Here, based on gene expression analysis, we show that MMP-9 is upregulated by Hes1 in common myeloid progenitors (CMPs). Analysis of promoter activity demonstrated that Hes1 upregulated MMP-9 by activating NF-kB. Analysis of 20 samples from CML-BC patients showed that MMP-9 was highly expressed in three, with two exhibiting high levels of Hes1 expression. Interestingly, MMP-9 deficiency impaired the cobblestone area-forming ability of CMPs expressing BCR-ABL and Hes1 that were in conjunction with a stromal cell layer. In addition, these CMPs secreted MMP-9, promoting the release of soluble Kit-ligand (sKitL) from stromal cells, thereby enhancing proliferation of the leukemic cells. In accordance, mice transplanted with CMPs expressing BCR-ABL and Hes1 exhibited high levels of sKitL as well as MMP-9 in the serum. Importantly, MMP-9 deficiency impaired the development of CML-BC–like disease induced by BCR-ABL and Hes1 in mouse BMT models. The present results suggest that Hes1 promotes the development of CML-BC, partly through MMP-9 upregulation in leukemic cells.

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