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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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High throughput sequencing of human HepG2 DNA immunoprecipitated with FOXA2, HNF4a and NRF2/GABP

ABSTRACT: In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus.

ORGANISM(S): Homo sapiens

SUBMITTER: Ola Wallerman

PROVIDER: E-MTAB-115 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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[E-MTAB-115] ChIP-seq for FOXA2 HNF4a and NRF2 / GABP in HepG2

Project description:In each cell type the expression of genes is regulated by the action of a large number of transcription factors, but so far we have only a rudimentary knowledge of the location of the gene regulatory elements where they bind. This can now be addressed with genome-wide ChIP experiments. In a previous ChIP-chip study of USF1 and USF2 we found evidence also of binding of GABP, FOXA2 and HNF4a within the enriched regions. Here we have applied ChIP-seq for these transcription factors and identified 3064 peaks of enrichment for GABP, 7266 for FOXA2 and 18783 for HNF4a. HNF4a and FOXA2 binding was found in at least half of the regions previously identified as bound by USF2 but not USF1, showing that they frequently bind the same regulatory elements. GABP peaks were found at transcription start sites whereas 94 % of FOXA2 and 90 % of HNF4a peaks were located at other positions. We developed a method based on the high resolution achieved by ChIP-seq to accurately define TFBS within peaks, and found the predicted sites to have an elevated conservation level compared to peak centers; however the majority of bindings were not evolutionary conserved. An unexpected interaction between HNF4a and GABP was seen at TSS, with as many as 1/3 of the HNF4a positive promoters being bound also by GABP, and co-immunoprecipitations show that these factors are in the same complex in the nucleus. ArrayExpress Release Date: 2009-06-10 Publication Title: Molecular interactions between HNF4a, FOXA2 and GABP identified at regulatory DNA elements through ChIP-sequencing Publication Author List: Ola Wallerman, Mehdi Motallebipour, Stefan Enroth, Kalicharan Patra, MadhuSudan Reddy Bysani, Jan Komorowski, Claes Wadelius Person Roles: submitter Person Last Name: Wallerman Person First Name: Ola Person Mid Initials: Person Email: ola.wallerman@genpat.uu.se Person Phone: Person Address: IGP, Rudbecklab Person Affiliation: Uppsala University

2011-02-05 | GSE25694 | GEO

Genome-wide Profiling of FOXA2 and POL2 binding in the mouse uterus [ChIP-Seq]

Project description:Forkhead box A2 (FOXA2) is a critical regulator of endometrial gland development in mice. In the adult mouse uterus, FOXA2 is expressed solely in the GE cells of the endometrium. Conditional deletion of Foxa2 after birth in the uterus, using the progesterone receptor Cre mouse (PgrCre), impeded gland development, thereby rendering the adult mouse infertile due to defects in blastocyst implantation stemming from a lack of endometrial glands and their secretions. As a first step to begin understanding the FOXA2 function in the endometrial glands of the uterus, genome-wide investigation of in vivo FOXA2 and RNA polymerase II (POL2) binding target regions in the neonatal and adult uterus was determined by chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-Seq). In order to determine the transcriptional regulatory networks mediating FOXA2 regulation of endometrial gland development and function, chromatin immunoprecipitation and massively parallel sequencing (ChIP-Seq) was used to create a genome-wide profile of in vivo FOXA2-binding sites in the developing (PD 12) and adult (DOPP 2.5 and 3.5) mouse uterus.

2013-12-01 | E-GEOD-48238 | biostudies-arrayexpress

FOXA2 regulates a network of genes involved in critical functions of intestinal epithelia

Project description:Background and Aims: The forkhead box A (FOXA) family of pioneer transcription factors is critical for the development of many endoderm-derived tissues including the lung and the liver. Here we investigate the role of FOXA2 in regulating intestinal epithelial cell function. Methods: ChIP-seq was used to identify FOXA2 binding sites genome-wide. Targets of FOXA2 were validated using ChIP-qPCR and siRNA-mediated depletion of FOXA1/2 followed by RT-qPCR. A luciferase-based assay was used to measure intracellular cAMP after FOXA1/2 modulation.Results: Peaks of FOXA2 occupancy were frequent at loci contributing to gene ontology pathways of regulation of cell migration, cell motion, and plasma membrane function. Depletion of both FOXA1 and FOXA2 led to a significant reduction in the expression of multiple transmembrane proteins including ion transporters. One of the targets was the adenosine A2B receptor, and reduced receptor mRNA levels were associated with a functional decrease in intracellular cAMP. We also observed that 30% of FOXA2 binding sites contained a GATA motif and that FOXA1/A2 depletion reduced GATA-4, but not GATA-6 protein levels. Conclusions: These data show that FOXA2 plays a critical role in regulating intestinal epithelial cell function. FOXA2 depletion affects the expression of ion transporters and other transmembrane proteins, which form a network essential for maintaining normal ion and solute transport. Moreover, we show that the FOXA and GATA families of transcription factors may work cooperatively to regulate gene expression genome-wide. To determine the role of FOXA2 in regulating gene expression in intestinal epithelial cells, ChIP-seq was performed for FOXA2 in Caco2 (colorectal adenocarcinoma) cells.

2015-08-06 | E-GEOD-66218 | biostudies-arrayexpress

Genome-wide analyses in neuronal cells reveal that USF transcription factors regulate lysosomal gene expression [ChIP-chip]

Project description:The upstream stimulating factors (USFs) USF1 and USF2 are ubiquitously expressed transcription factors characterized by a conserved basic helix-loop-helix leucine zipper DNA-binding domain. They form homo- or heterodimers and recognize E-box motifs to modulate gene expression. They are known to regulate diverse cellular functions including the cell cycle, immune response and glucose-lipid metabolism, but their roles in neuronal cells remain to be clarified. Here, we performed chromatin immunoprecipitation of USF1 from mouse brain cortex preparations. Subsequent promoter array analysis (ChIP-chip) indicated that USF1 exclusively bound to the CACGTG E-box motifs in the proximal promoter regions. Importantly, functional annotation of the USF1-binding targets revealed an enrichment of genes related to lysosomal functions. Gene expression arrays using a neuronal cell line subsequently revealed that knockdown of USFs deregulated lysosomal gene expression. Altered expression was validated by quantitative RT-PCR, supporting the conclusion that USFs regulate lysosomal gene expression. Furthermore, USFs knockdown slightly increased LysoTracker staining, implying a role for USFs in modulating lysosomal homeostasis. Together, our comprehensive, genome-scale analyses identified lysosomal genes as targets of USFs in neuronal cells, suggesting a potential additional pathway of lysosomal regulation. ChIP-chip analysis of USF1 and NF-Y in mouse brain cortex. To identify downstream targets of USF1 and NF-Y in neuronal cells, they were chromatin-immunoprecipitated from mouse brain cortical lysates. The obtained chromatin DNAs were labeled with biotin and hybridized on Affymetrix Mouse Promoter 1.0R Array.

2016-01-08 | E-GEOD-76616 | biostudies-arrayexpress

ChIP-seq of NRF2 in Fh1-KO cells

Project description:To identify the genomic location of FOXA2 in and Fh1-KO cells.

2023-06-12 | E-MTAB-13042 | biostudies-arrayexpress

Identification of candidate FOXA2-regulated genes in the adult mouse uterus

Project description:To identify candidate genes regulated by forkhead transcription factor box A2 (FOXA2) in the uterus, control and Foxa2-deleted uteri were collected at day of pseudopregnancy (DOPP) 3.5 (DOPP 0.5= vaginal plug). Microarray analysis identified differentially expressed genes in the Foxa2-deleted as compared to control uteri that are candidiate FOXA2-regulated genes in the uterus. Whole uteri (control wild type n=4; Foxa2-deleted n=4) were analyzed for differences in their transcriptome using a mouse microarray.

2013-12-01 | E-GEOD-48339 | biostudies-arrayexpress

Homo sapiens

Project description:[E-MTAB-115] ChIP-seq for FOXA2 HNF4a and NRF2 / GABP in HepG2

| PRJNA135845 | ENA

Analysis of FoxA2 occupancy in mouse liver with endoderm ChIP-chip array

Project description:Understanding how silent genes can be competent for activation provides insight into development as well as cellular reprogramming and pathogenesis. We performed genomic location analysis of the pioneer transcription factor FoxA in the adult liver and found that about one-third of the FoxA bound sites are near silent genes, including genes without detectable RNA polymerase II. Virtually all of the FoxA-bound silent sites are within extended conserved sequences, suggesting possible function. Such sequences are enriched in motifs for transcriptional repressors, including for Rfx1. We found one such target site containing functional FoxA and Rfx1 sites is a cryptic enhancer 7 kb downstream of the Cdx2 gene, the latter being an effector of esophageal metaplasia. Indeed, Rfx1 sites restrict transcriptional activation by FoxA at the +7 kb Cdx2 element. Furthermore, Rfx1 expression in the esophageal epithelium becomes extinguished during its metaplastic progression to carcinoma. We propose that motif analysis of other transcription factors bound to silent genes can reveal unanticipated regulatory networks that provide insights into reprogramming and oncogenic progression. We analyzed FOXA2 occupancy in a mouse liver sample. We ran three competitive hybridizations: (i) FOXA2 vs IgG, (ii) FOXA2 vs input, and (iii) IgG vs input.

2011-07-18 | E-GEOD-23551 | biostudies-arrayexpress

ChIPmentation of FOXA2 in Fh1-WT and Fh1-KO cells

Project description:To identify the genomic location of FOXA2 in Fh1-WT and Fh1-KO cells.

2022-09-01 | E-MTAB-11785 | biostudies-arrayexpress

Chromatin immunoprecipitation of human cell line HepG2 with anti-Histone H3 acetyl K9/14, USF1 antibody, USF2 antibody and normal rabbit IgG

Project description:Whole genome ChIP-chip study using human liver cell line HepG2 and anti-Histone H3 acetyl K9/14 (06-599); USF1 antibody (H-86, sc-8983); USF2 antibody (C-20, sc-862) and normal rabbit IgG (12-370). Three completely independent biological replicates were performed for each antibody, obtaining the corresponding input as total genomic DNA reference. Hybridizations were performed using Affymetrix GeneChip Human Tiling 2.0R Array set (7 arrays set).

2007-11-30 | E-TABM-314 | biostudies-arrayexpress

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