Dataset Information


Genome-wide DNA-binding profile of HNF4A and genome occupancy of the histone modifications H3K4me1, H3K27ac in kidneys from Bicc1 WT and KO mice by ChIPseq.

ABSTRACT: 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,] 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.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus  

SUBMITTER: Daniel Constam   Teresa Didonna  

PROVIDER: E-MTAB-6424 | ArrayExpress | 2020-01-20



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Network analysis of a Pkd1-mouse model of autosomal dominant polycystic kidney disease identifies HNF4α as a disease modifier.

Menezes Luis F LF   Zhou Fang F   Patterson Andrew D AD   Piontek Klaus B KB   Krausz Kristopher W KW   Gonzalez Frank J FJ   Germino Gregory G GG  

PLoS genetics 20121129 11

Autosomal Dominant Polycystic Kidney Disease (ADPKD; MIM ID's 173900, 601313, 613095) leads to end-stage kidney disease, caused by mutations in PKD1 or PKD2. Inactivation of Pkd1 before or after P13 in mice results in distinct early- or late-onset disease. Using a mouse model of ADPKD carrying floxed Pkd1 alleles and an inducible Cre recombinase, we intensively analyzed the relationship between renal maturation and cyst formation by applying transcriptomics and metabolomics to follow disease pro  ...[more]

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