ChIP-seq analysis of adult human kidney cortex
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA531890 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8875020.fastq.gz | Fastqsanger.gz | |||
| SRR8875021.fastq.gz | Fastqsanger.gz | |||
| SRR8875022.fastq.gz | Fastqsanger.gz | |||
| SRR8875013.fastq.gz | Fastqsanger.gz | |||
| SRR8875023.fastq.gz | Fastqsanger.gz |
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Project description:Human kidney was obtained from the University of Wisconsin Madison Organ Procurement Program from a deceased 69 year old female patient and the cortex was dissected from 3 different cortex locations. Associated publication abstract: Targeted genomic deletions identify diverse enhancer functions and generate a kidney-specific, endocrine-deficient Cyp27b1 pseudo-null mouse Vitamin D3 is terminally bioactivated in the kidney to 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) via cytochrome P450 family 27 subfamily B member 1 (CYP27B1), whose gene is regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and 1,25(OH)2D3. Our recent genomic studies in the mouse have revealed a complex kidney-specific enhancer module within the introns of adjacent methyltransferase like 1 (Mettl1) and Mettl21b that mediate basal and PTH induced expression of Cyp27b1 and FGF23- and 1,25(OH)2D3-mediated repression. Gross deletion of these segments in mice has severe consequences on Cyp27b1 regulation and skeletal phenotype, but does not affect Cyp27b1 expression in non-renal target cells (NRTCs). Here, we report a bimodal activity in the Mettl1 intronic enhancer with components responsible for PTH-mediated Cyp27b1 induction and 1,25(OH)2D3-mediated repression and additional activities, including FGF23 repression, within the Mettl21b enhancers. Deletion of both submodules eliminated basal Cyp27b1 expression and regulation in the kidney, leading to systemic and skeletal phenotypes similar to those of Cyp27b1-null mice. However, basal expression and lipopolysaccharide-induced regulation of Cyp27b1 in NRTCs was unperturbed. Importantly, dietary normalization of calcium, phosphate, PTH, and FGF23 rescued the skeletal phenotype of this mutant mouse, creating an ideal in vivo model to study non-renal 1,25(OH)2D3 production in health and disease. Finally, we confirmed a conserved chromatin landscape in human kidney that is similar to that in mouse. These findings define a finely balanced homeostatic mechanism involving PTH and FGF23 together with protection from 1,25(OH)2D3 toxicity that is responsible for both adaptive vitamin D metabolism and mineral regulation.
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Project description:We report gene expression (RNA-seq) from macro-dissected human kidney cortex and medulla from 3 individuals
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Project description:O-GlcNAcylation is a global post translational modification. The purpose of this study is to investigate the role of O-GlcNAcylation in mice kidney proximal tubules. We used drug-inducible proximal tubular cells specific O-GlcNAc transferase (Ogt) KO mice (PTEC-Ogt KO). In this proteomic analysis, we compared kidney cortex from fasted PTEC-Ogt KO and Control mice.
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Project description:We report gene expression (RNA-seq) from macro-dissected human kidney cortex and medulla from 3 individuals. The samples were from patients undergoing kidney removal for tumors, but the tissues used in the study itself were normal tissue/cultured cells not involved by tumor.
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Project description:We report chromatin conformation (Hi-C) maps from macro-dissected human kidney cortex and medulla from 1 individual
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