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Genome-wide chromatin accessibility (ATAC-Seq) of primary murine nephron progenitor cells.

ABSTRACT: Genome-wide chromatin accessibility (ATAC-Seq) of primary murine nephron progenitor cells.

PROVIDER: PRJNA930634 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23314930_1.fastq.gz	Fastqsanger.gz
	SRR23314930_2.fastq.gz	Fastqsanger.gz
	SRR23314931_1.fastq.gz	Fastqsanger.gz
	SRR23314931_2.fastq.gz	Fastqsanger.gz
	SRR23314932_1.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin accessibility (ATAC-Seq) of primary murine nephron progenitor cells.

Project description:This series contains ATAC-Seq data generated from mouse nephron progenitor cells (NPCs) isolated from different strains/mutants and developmental timepoints as indicated.

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Project description:This series contains Hi-C data generated from postnatal day 0 mouse nephron progenitor cells (NPCs) isolated from three different genotypes representing control, low and high nephron number mouse lines.

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Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development [ATAC-Seq]

Project description:Mammalian nephron progenitors undergo transcriptional changes over the course of nephrogenesis that sensitize them to signals for differentiation over time. This increases the rate at which they exit their multipotent, self-renewing mesenchymal state and become differentiated epithelial cells, ultimately depleting the progenitor population and leading to the cessation of nephrogenesis. We hypothesized that changes in chromain accessibility and miRNA expression would accompany these transcriptional changes, and that regions of changing chromatin accessibiltiy could reveal chaning regulatory features such as enhancers, including some that affect miRNA expression. To test this, we pooled kidneys from wild-type mouse litters sacrificed at embryonic day 14.5 (E14.5) and post-natal day zero (P0) using positive selection for the surface protein Integrin alpha 8 (Itga8), then sequenced the assay for transposase-accessible chromatin (ATAC-seq) using 50,000 cells, and used the remaining cells for small RNA sequencing (smRNA-seq). ATAC-seq libraries were generated using the Nextera DNA Flex Library Prep Kit (Illumina FC-121-1030) with modifications according to a previously published method (Buenrostro et al., 2013), and all sequencing was performed using an Illumina NextSeq500 by the Health Sciences Sequencing Core at UPMC Children's Hospital of Pittsburgh.

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Mapping open chromatin in mouse nephron progenitor cells

Project description:To delineate the epigenomic profile of the Six2+ mouse nephron progenitor cells, we mapped open chromatin using ATAC-Seq in Six2+ cells from E16.5 mouse kidneys.

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Gene Expression and Chromatin Accessibility of Nephron Progenitor Cells in Mice

Project description:Gene Expression and Chromatin Accessibility of Nephron Progenitor Cells in Mice

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LGR6 marks nephron progenitor cells

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p53 Enables Self Renewal of Nephron Progenitor Cells

Project description:p53 limits the self-renewing ability of a variety of stem cells. Here, contrary to its classical role in restraining cell proliferation, we demonstrate a divergent function of p53 in maintenance of self-renewal of the nephron progenitor population in the embryonic mouse kidney. p53-null nephron progenitor cells (NPC) exhibit progressive loss of the self-renewing progenitor niche in the cap mesenchyme, identified by Cited1 and Six2 expression, and loss of cap integrity. Nephron endowment is regulated by NPC availability and their differentiation to nephrons. Quantitatively, the Six2p53-/- cap has 30% fewer Six2GFP+ cells. While the apoptotic index is unchanged the proliferation index is significantly lower, in accordance with cell cycle analysis data showing less mutant Six2p53-/-;GFP+ cells in S and G2/M phases in comparison to Six2p53+/+;GFP+ cells. The mutant kidneys also show nephron deficit and decreased Fgf8 expression. To investigate the underlying changes in gene expression in the cap mesenchyme that contribute to the Six2p53-/- phenotype, we utilized RNA-Seq for transcriptome comparison. Top biological processes affected by p53 loss are development and morphogenesis, cell adhesion/migration, cell survival and metabolism. Cells from the mutant CM showed increased cellular ROS levels as well as deregulated expression of energy metabolism and mitochondrial genes suggesting metabolic dysfunction. Adhesion defects are visualized by decreased immunostaining of adhesion marker NCAM, and may possibly contribute to the differentiation defect as well. Altogether our data suggest a novel role for p53 in enabling self-renewal of the NPC and preservation of the progenitor niche, and thus regulating nephron endowment. mRNA profiles of wild-type (WT) and conditional p53 knockout (KO) of Six2+ mouse nephron progenitor cells (NPC) at embryonic day 15.5

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Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development

Project description:Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development

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Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number

Project description:The regulation of final nephron number in the kidney is poorly understood. However, cessation of nephron formation occurs when the self-renewing nephron progenitor population commits to differentiation. Transcription factors within this progenitor population, such as SIX2, are assumed to control expression of genes promoting self-renewal such that homozygous Six2 deletion results in premature commitment and an early halt to kidney development. In contrast, Six2 heterozygotes were assumed to be unaffected. Using quantitative morphometry, we demonstrate here a paradoxical 18% increase in ureteric branching and final nephron number in Six2 heterozygotes, despite evidence for reduced levels of SIX2 protein and transcript. This is accompanied by a clear shift in nephron progenitor identity with a distinct subset of progenitor genes, including Cited1 and Meox1, downregulated, while others were unaffected. The net result was an increase in nephron progenitor proliferation, as assessed by elevated EDU labelling, an increase in MYC protein and transcriptional upregulation of MYC target genes. Reducing proliferation by introducing Six2 heterozygosity onto the Fgf20-/- background resulted in premature differentiation of the progenitor population. Overall, this data demonstrates a unique dose response of the nephron progenitors to the level of SIX2 protein in which the role of SIX2 in progenitor proliferation versus self-renewal is separable.

2017-12-31 | GSE103219 | GEO

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