Genome-wide mapping of Hnf4a binding sites in the newborn mouse kidneys
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA605010 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11031277.fastq.gz | Fastqsanger.gz | |||
| SRR11031278.fastq.gz | Fastqsanger.gz | |||
| SRR11031279_1.fastq.gz | Fastqsanger.gz | |||
| SRR11031279_2.fastq.gz | Fastqsanger.gz | |||
| SRR11031280_1.fastq.gz | Fastqsanger.gz |
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Project description:Hnf4a is specifically expressed in developing proximal tubule cells in the newborn mouse kidney. In order to identify direct target genes of Hnf4a in the developing proximal tubules, we performed ChIP-Seq of Hnf4a in the mouse kidneys at P0.
2020-11-12 | GSE144824 | GEO
Project description:Mutations in Bicaudaul C 1 (BICC1), evolutionary conserved RNA-binding protein, cause renal cysts in mice and humans. These renal cysts are reminiscent of Polycystic Kidney Disease (PKD). How BICC1 is involved in the pathogenesis of polycystic kidney disease is still unknown. Recent studies highlighted that HNF4A plays a role in the regulation of metabolic pathways deregulated in this renal disease. Moreover, Menezes et al. [2012, https://doi.org/10.1371/journal.pgen.1003053] showed that combined kidney inactivation of Hnf4a and Pkd1 in mice significantly worsened the cystic phenotype. Here we investigated whether the DNA binding and transcriptional activity of HNF4A might be deregulated in kidneys from Bicc1 mouse model of polycystic kidney disease. HNF4A, H3K27ac, H3K4me1 ChIPseq experiments were performed in kidneys from male and female Bicc1 WT and KO mice. From the contralateral kidneys of the same animals used for the ChIPseq experiments, the total RNA was extracted for gene expression profiling by RNAseq. The RNAseq data was used to support the ChIP-seq analysis and to reveal deregulated pathways in BICC1 mutants.
2020-01-20 | E-MTAB-6424 | biostudies-arrayexpress
Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4A binding regions under TGF-β stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4A bindings. MIXL1 was identified as a new combinatorial target of HNF4A and Smad2/3, and both the HNF4A protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4A on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway. HepG2 cells were treated with TGF-beta for 1.5 h or left untreated. anti-HNF4A ChIP-seq was performed. One lane was used for each sample.
2011-06-08 | E-GEOD-28845 | biostudies-arrayexpress
Project description:Specific regulation of target genes by transforming growth factor-β (TGF-β) in a given cellular context is determined in part by transcription factors and cofactors that interact with the Smad complex. In the present study, we determined Smad2 and Smad3 (Smad2/3) binding regions in the promoters of known genes in HepG2 hepatoblastoma cells, and compared them to those in HaCaT epidermal keratinocytes to elucidate the mechanisms of cell type- and context-dependent regulation of transcription induced by TGF-β. Our results show that 81% of the Smad2/3 binding regions in HepG2 cells were not shared with those found in HaCaT cells. Hepatocyte nuclear factor 4α (HNF4α) is expressed in HepG2 cells, but not in HaCaT cells, and the HNF4α binding motif was identified as an enriched motif in the HepG2-specific Smad2/3 binding regions. ChIP-sequencing analysis of HNF4A binding regions under TGF-β stimulation revealed that 32.5% of the Smad2/3 binding regions overlapped HNF4A bindings. MIXL1 was identified as a new combinatorial target of HNF4A and Smad2/3, and both the HNF4A protein and its binding motif were required for the induction of MIXL1 by TGF-β in HepG2 cells. These findings generalize the importance of binding of HNF4A on Smad2/3 binding genomic regions for HepG2-specific regulation of transcription by TGF-β, and suggest that certain transcription factors expressed in a cell-type-specific manner play important roles in the transcription regulated by the TGF-β-Smad signaling pathway.
2011-06-08 | GSE28845 | GEO
Project description:HNF4a has been shown to be critical for hepatocyte differentiation from iPS cells.
2019-01-28 | GSE104613 | GEO
Project description:The transcriptional regulation of drug-metabolizing enzymes and transporters (here collectively referred to as DMEs) in the developing proximal tubule is not well understood. As in the liver, DME regulation in the PT may be mediated through nuclear receptors which are thought to “sense” deviations from homeostasis by being activated by ligands, some of which are handled by DMEs, including drug transporters. Systems analysis of transcriptomic data during kidney development predicted a set of upstream transcription factors, including Hnf4a and Hnf1a, as well as Nr3c1 (Gr), Nfe2l2 (Nrf2), Ppara, and Tp53. Motif analysis of cis-regulatory further suggested that Hnf4a and Hnf1a are the main transcriptional regulators in the PT. Available expression data from tissue-specific Hnf4a KO tissues revealed that distinct subsets of DMEs were regulated by Hnf4a in a tissue-specific manner. ChIP-seq was performed to characterize the PT-specific binding sites of Hnf4a in rat kidneys at three developmental stages (prenatal, immature, adult), which further supported a major role for Hnf4a in regulating PT gene expression, including DMEs. In ex vivo kidney organ culture, an antagonist of Hnf4a (but not a similar inactive compound) led to predicted changes in DME expression, including among others Fmo1, Cyp2d2, Cyp2d4, Nqo2, as well as organic cation transporters and organic anion transporters Slc22a1(Oct1), Slc22a2 (Oct2), Slc22a6 (Oat1), Slc22a8(Oat3), and Slc47a1(Mate1). Conversely, overexpression of Hnf1a and Hnf4a in primary mouse embryonic fibroblasts (MEFs), sometimes considered a surrogate for mesenchymal stem cells, induced expression of several of these proximal tubule DMEs, as well as epithelial markers and a PT-specific brush border marker Ggt1. These cells had organic anion transporter function. Taken together, the data strongly supports a critical role for HNF4a and Hnf1a in the tissue-specific regulation of drug handling and differentiation toward a PT cellular identity. Hnf4a binding was examined in rat kidneys at three timepoints (E20, P13 and Adult) and p300 binding was examined in adult rat kidney cortex tissue using ChIP-seq. Four corresponding input DNA samples were used as controls for peak calling.
2014-01-01 | E-GEOD-50815 | biostudies-arrayexpress
Project description:HNF4A mRNA cycles over the coure of 24 h. To understand whether the chromatin binding of the transcription factor is also rhythmic, we performed ChIP-seq for HNF4A using mouse liver samples of ZT4 and ZT16. By analysing this dataset, we conclude that HNF4A binds chromatin much more robustly during the evening ( at ZT16).
2018-08-02 | GSE118007 | GEO
Project description:Genome-wide map of binding sites for HNF4a during hepatic specification of iPS cells
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Project description:The glucocorticoid receptor (GR) is a nuclear hormone receptor critical to the regulation of energy metabolism and the inflammatory response. The actions of GR are highly dependent on cell type and environmental context. Here, we demonstrate the necessity for liver lineage-determining factor hepatocyte nuclear factor 4A (HNF4A) in defining liver-specificity of GR action. In normal mouse liver, the HNF4 motif lies adjacent to the glucocorticoid response element (GRE) at GR binding sites found within regions of open chromatin. In the absence of HNF4A, the liver GR cistrome is remodelled, with both loss and gain of GR recruitment evident. Loss of chromatin accessibility at HNF4A-marked sites leads to loss of GR binding at weak GRE motifs. GR binding is gained at sites characterised by strong GRE motifs, which typically show GR recruitment in non-liver tissues. The functional importance of these HNF4A-regulated GR sites is further demonstrated by evidence of an altered transcriptional response to glucocorticoid treatment in the Hnf4a-null liver.
2022-01-20 | E-MTAB-10266 | biostudies-arrayexpress