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Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha

ABSTRACT: Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha

PROVIDER: PRJNA354702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5045900.fastq.gz	Fastqsanger.gz
	SRR5047250.fastq.gz	Fastqsanger.gz
	SRR5047260.fastq.gz	Fastqsanger.gz
	SRR5047270.fastq.gz	Fastqsanger.gz
	SRR5045901.fastq.gz	Fastqsanger.gz

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Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha.

Project description:Microbiota influence diverse aspects of intestinal physiology and disease in part by controlling tissue-specific transcription of host genes. However, host genomic mechanisms mediating microbial control of intestinal gene expression are poorly understood. Hepatocyte nuclear factor 4 (HNF4) is the most ancient family of nuclear receptor transcription factors with important roles in human metabolic and inflammatory bowel diseases, but a role in host response to microbes is unknown. Using an unbiased screening strategy, we found that zebrafish Hnf4a specifically binds and activates a microbiota-suppressed intestinal epithelial transcriptional enhancer. Genetic analysis revealed that zebrafish hnf4a activates nearly half of the genes that are suppressed by microbiota, suggesting microbiota negatively regulate Hnf4a. In support, analysis of genomic architecture in mouse intestinal epithelial cells disclosed that microbiota colonization leads to activation or inactivation of hundreds of enhancers along with drastic genome-wide reduction of HNF4A and HNF4G occupancy. Interspecies meta-analysis suggested interactions between HNF4A and microbiota promote gene expression patterns associated with human inflammatory bowel diseases. These results indicate a critical and conserved role for HNF4A in maintaining intestinal homeostasis in response to microbiota.

| S-EPMC5495071 | biostudies-literature

Proteomic analysis of native hepatocyte nuclear factor-4{alpha} (HNF4{alpha}) isoforms, phosphorylation status, and interactive cofactors.

Project description:Hepatocyte nuclear factor-4α (HNF4α, NR2A1) is a nuclear receptor which has a critical role in hepatocyte differentiation and the maintenance of homeostasis in the adult liver. However, a detailed understanding of native HNF4α in the steady state remains to be elucidated. Here we report the native HNF4α isoforms, phosphorylation status and complexes in the steady state, as shown by shotgun proteomics in HepG2 hepatocarcinoma cells. Shotgun proteomic analysis revealed the complexity of native HNF4α, including multiple phosphorylation sites and inter-isoform heterodimerization. The associating complexes identified by label-free semi-quantitative proteomic analysis include the following: the DNA-dependent protein kinase catalytic subunit, histone acetyltransferase complexes, mRNA splicing complex, other nuclear receptor coactivator complexes, the chromatin remodeling complex, and the nucleosome remodeling and histone deacetylation complex. Among the associating proteins, GRB10 interacting GYF protein 2 (GIGYF2, PERQ2) is a new candidate cofactor in metabolic regulation. Moreover, an unexpected heterodimerization of HNF4α and Hepatocyte nuclear factor-4γ was found. A biochemical and genome-wide analysis of transcriptional regulation showed that this heterodimerization activates gene transcription. The genes thus transcribed include the cell death-inducing DEF45-like effector b (CIDEB) gene, which is an important regulator of lipid metabolism in the liver. This suggests that the analysis of the distinctive stoichiometric balance of native HNF4α and its cofactor complexes described here is important for an accurate understanding of transcriptional regulation. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.

2010-12-22 | E-GEOD-18990 | biostudies-arrayexpress

Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha

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

2017-03-27 | GSE90462 | GEO

Hepatocyte nuclear factor 1β binding in E14.5 kidney

Project description:Hepatocyte nuclear factor 1β binding in E14.5 kidney

| PRJNA844065 | ENA

Effect of the twelve isoforms of Hepatocyte nuclear factor 4 alpha on HCT116 cell line transcriptome

Project description:Effect of the twelve isoforms of Hepatocyte nuclear factor 4 alpha on HCT116 cell line transcriptome

| PRJNA517705 | ENA

Proteomic analysis of native hepatocyte nuclear factor-4{alpha} (HNF4{alpha}) isoforms, phosphorylation status, and interactive cofactors.

2010-12-22 | GSE18990 | GEO

Microbiota regulate intestinal epithelial gene expression by suppressing the transcription factor Hepatocyte nuclear factor 4 alpha (zebrafish RNA-seq)

Project description:We performed RNA-seq from 6 days post fertilization hnf4a-/- and hnf4a+/+ zebrafish larval digestive tracts raised in the absence (Germ Free, GF) or presence (Conventionalized, CV) of microbiota. We found that zebrafish hnf4a activates almost half of the microbiota-suppressed genes, indicating that the microbiota supress Hnf4a trans-activity. We also provide evidence suggesting that microbial suppression of Hnf4a may contribute to IBD pathogenesis.

2017-03-27 | GSE90446 | GEO

Impact of high fat diet and hepatocyte nuclear factor four alpha loss on hepatic gene expression in mice.

Project description:Impact of high fat diet and hepatocyte nuclear factor four alpha loss on hepatic gene expression in mice.

| PRJNA564330 | ENA

Hepatocyte nuclear factor 1β binding in E14.5 kidney

Project description:HNF-1β mutations are one of the most common single-gene mutations that underlie kidney developmental disease. Hepatocyte nuclear factor 1β (HNF-1β) is essential for kidney development, but its functions in kidney development are incompletely understood. We identified 8284 HNF-1β binding sites using ChIP-sequencing. The majority of these peaks map to promoter (26%), intron (34%) or distal intergenic regions (37.4%) of the mouse genome. 61% of peaks map to protein coding genes, 12% map to long-noncoding RNAs, and 2% map to miRNAs.

2022-10-20 | GSE205189 | GEO

Impact of high fat diet and hepatocyte nuclear factor four alpha loss on hepatic gene expression in mice.

Project description:The transcription factor hepatocyte nuclear factor four alpha (Hnf4a) has various isoforms, one of which (P1-Hnf4a) is expressed in adult liver, where it functions as a tumor suppressor by providing circadian restrains at genes promoting cell proliferation and epithelial to mesenchymal transition. High fat diet feeding promotes the loss of nuclear P1-Hnf4a activity and a gain in the pro-proliferative P2-Hnf4a isoform, which does not function as a tumor suppressor, nor provide similar circadian restraint at cell cycle-promoting genes. P2-Hnf4a is found in all Hnf4a-positive hepatocellular carcinoma. Purpose: To determine whether inducible loss of hepatic Hnf4a followed by high fat feeding predisposes a liver to hepatocellular carcinoma. Methods: Hepatic Hnf4a was inducibly knocked out in mice at six weeks of age ("H4LivKO") followed by vivarium chow ("H4LivKOVC") or high fat feeding ("H4LivKOHF")at 8 weeks of age. Control, littermate wild-type mice (WT) were also treated with tamoxifen at six weeks of age, but since they lacked the Cre transgene, Hnf4a expression remained intact. Control mice were divided into the same feeding groups as H4LivKO mice ("WTVC" and "WTHF"). Livers were harvested at 38 weeks of age and liver tissue was flash frozen in liquid nitrogen. RNA was extracted from frozen liver tissue using Trizol, and purified RNA was submitted to Novogene for quality control and RNA-seq analysis using a 250-300 bp insert cDNA library and Illumina Platform sequencing.

2019-09-07 | GSE137051 | GEO

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