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Single cell RNA-Seq of sorted nephron progenitor cells from pooled mouse kidneys

ABSTRACT: Single cell RNA-Seq of sorted nephron progenitor cells from pooled mouse kidneys

PROVIDER: PRJNA540758 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9002410_1.fastq.gz	Fastqsanger.gz
	SRR9002410_2.fastq.gz	Fastqsanger.gz
	SRR9002420_1.fastq.gz	Fastqsanger.gz
	SRR9002420_2.fastq.gz	Fastqsanger.gz
	SRR9002411_1.fastq.gz	Fastqsanger.gz

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Single cell RNA-Seq of sorted nephron progenitor cells from pooled mouse kidneys

Project description:Kidneys from multiple litters of Six2GFP+ E14.5 mouse embryos were pooled into three replicate tubes and dissociated in parallel. Six2GFP+ cells were isolated and processed for single cell sequencing using 10x Genomics technology. This resulted in a dataset of 7844 single cells representing the nephron progenitor population of the mouse kidney.

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Stromal Fat4 acts non-autonomously with Dachsous1/2 to restrict the nephron progenitor pool

Project description:Regulation of the balance between progenitor self-renewal and differentiation is critical to development. In the mammalian kidney, reciprocal signaling between three lineages (stromal, mesenchymal and ureteric) ensures correct nephron progenitor self-renewal and differentiation. Loss of either the atypical cadherin Fat4 or its ligand Dachsous1 (Dchs1) results in expansion of the mesenchymal nephron progenitor pool, called the condensing mesenchyme (CM). This has been proposed to be due to misregulation of the Hippo kinase pathway transcriptional co-activator YAP. Here, we use tissue-specific deletions to prove that Fat4 acts non-autonomously in the renal stroma to control nephron progenitors. We show that loss of Yap from the CM in a Fat4-null background does not reduce the expanded CM, indicating Fat4 regulates the CM independent of YAP. Analysis of Six2-/-;Fat4-/- double mutants demonstrates that excess progenitors in Fat4 mutants are dependent on Six2, a critical regulator of nephron progenitor self-renewal. Electron microscopy reveals that cell organization is disrupted in Fat4 mutants. Gene expression analysis demonstrates that the expression of Notch and FGF pathway components are altered in Fat4 mutants. Finally, we show that Dchs1, and its paralog Dchs2 function in a partially redundant fashion to regulate the number of nephron progenitors. Our data supports a model in which FAT4 in the stroma binds to DCHS1/2 in the CM to restrict progenitor self-renewal. A total of 3 Fat4-/- mutant embryos and 3 wildtype (Fat4+/+) control embryos were examined. Two kidneys from each embryo was used thereby yielding a total of 6 Fat4-/- mutant kidneys and 6 Fat4+/+ wildype kidneys. All kidneys examined were at E13.5.

2015-08-01 | E-GEOD-70452 | biostudies-arrayexpress

Von Hippel-Lindau Acts as a Metabolic Switch Controlling Nephron Progenitor Differentiation

Project description:RNA sequencing was performed on VHLNP+/- and VHLNP-/- E17.5 isolated nephron progenitors. E17.5 kidneys were dissected and screened using the GFP expression. Dissected kidneys that expressed GFP were dissociated into single cell suspensions and FACS sorted; each sample consisted of approximately 150,000 pooled nephron progenitor cells. RNA was extracted using the RNeasy Micro Kit (Qiagen). The Health Sciences Sequencing Core at Children’s Hospital of Pittsburgh performed library construction and RNA sequencing (single-end reads, 75bp). Bioinformatics quality control was performed using FastQC (version 0.11.5), and adapters were trimmed using BBDuk from the BBMap software package (version 37.41). Reads were aligned to transcripts assembled from the mm10 genome (GRCm38, GENCODE M17 ) using the Spliced Transcripts Alignments to a Reference software package (STAR, version 2.5.3a). Reads aligned to known transcripts were counted using the Bioconductor GenomicAlignments R package (version 1.10.1), and differential expression between VHLNP+/- and VHLNP-/- kidney samples was calculated using DESeq2 (version 1.18.1). Expression levels of 245 genes were identified as significantly altered between VHLNP+/- and VHLNP-/- samples (padj <= 0.05, fc > 2).

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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

2015-02-16 | E-GEOD-56253 | biostudies-arrayexpress

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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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FACS-sorted Six2-positive nephron progenitor cells at embryonic day 15.5: wildtype (WT) vs. conditional HDAC1&2-null (MUT)

Project description:Transcriptional profiling of FACS-sorted Six2-positive nephron progenitor cells from Six2CreEGFP mice without (WT) or with (MUT) homozygously floxed HDAC1 and HDAC2 alleles at the age of embryonic day 15.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of HDAC1&2 in the nephron progenitor population and successive changes to the series of events in kidney development.

2018-05-08 | GSE84305 | GEO

Whole kidneys at embryonic day 16.5: wildtype (WT) vs. conditional Dot1-knockout (KO) from Six2-positive nephron progenitor cells (NPC)

Project description:Transcriptional profiling of whole kidneys from Six2CreEGFP mice without (WT) or with (KO) homozygously floxed DOT1 alleles at the age of embryonic day 16.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of DOT1 gene in the nephron progenitor population (Six2 positive) and successive changes to the series of events in kidney development.

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Project description:To identify novel transcriptional targets following Qpc inactivation. We deleteted Qpc in SIX2 nephron progenitor cells using a Six2-eGFP/cre BAC transgene. We compared SIX2-expressing progenitors from Six2-Qpc-/- kidneys with control (Six2-Qpc+/-) embryonic kidneys at E18.5.

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Transcriptional profile of mouse nephron progenitor cells

Project description:In developing mammalian kidney, nephron progenitor cells (NPC) give rise to all cells in mature nephrons. Expression of the transcription factor Six2 marks NPC in developing mouse kidneys. Within the Six2+ cell population, uncommitted NPC is marked by Cited1 expression. Towards the depletion of NPC in P2, most of the Cited1+ NPC is committed. Therefore, most of the Six2+ cells in kidney represents committed NPC. In order to explore the mechanism of NPC self-renewal and differentiation, hereby we generated transcriptionl profiles of uncommitted NPC (Cited1RFP+ cells from kidneys of E16.5 Cited1tagRFP transgenic mice) and committed NPC (Six2GFP+ cells from kidneys of P2 Six2TGC transgenic mice).

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