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

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

PROVIDER: PRJNA707117 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13863678_1.fastq.gz	Fastqsanger.gz
	SRR13863678_2.fastq.gz	Fastqsanger.gz
	SRR13863679_1.fastq.gz	Fastqsanger.gz
	SRR13863679_2.fastq.gz	Fastqsanger.gz
	SRR13863680_1.fastq.gz	Fastqsanger.gz

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

Project description:Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development [miRNA-Seq]

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Repression of interstitial cell identity in nephron progenitor cells by Pax2 establishes the nephron-interstitium lineage boundary throughout mammalian kidney development

Project description:The kidney contains the functional units, the nephrons, surrounded by the renal interstitium. Previously, we discovered that, once Six2-expressing nephron progenitor cells and Foxd1-expressing renal interstitial progenitor cells form at the onset of kidney development, descendant cells from these populations contribute exclusively to the main body of nephrons and renal interstitial tissues, respectively, indicating a lineage boundary between the nephron and renal interstitial compartments. Currently, it is unclear how lineages are regulated during kidney organogenesis. We demonstrate that nephron progenitor cells lacking Pax2 activity failed to differentiate into nephron cells, but can switch fates into renal interstitium cell types. These data suggest that Pax2 function maintains nephron progenitor cells by repressing transdifferentiation into renal interstitial cell states. Thus, the lineage boundary between the nephron and renal interstitial compartments is maintained by the Pax2 activity in nephron progenitor cells during kidney organogenesis.

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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.

2023-03-04 | GSE168339 | GEO

Chromatin accessibility and microRNA expression in nephron progenitor cells during kidney development [miRNA-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). smRNA-seq libraries were generated using the QIAseq miRNA library preparation kit (Qiagen 331502), and all sequencing was performed using an Illumina NextSeq500 by the Health Sciences Sequencing Core at UPMC Children's Hospital of Pittsburgh.

2023-03-04 | GSE168342 | GEO

Modeling kidney development, disease, and plasticity with clonal expandable nephron progenitor cells and nephron organoids

Project description:Nephron progenitor cells (NPCs) self-renew and differentiate into nephrons, the functional units of the kidney. Here we report manipulation of p38 and YAP activity creates a synthetic niche that allows the long-term clonal expansion of primary mouse and human NPCs, and induced NPCs (iNPCs) from human pluripotent stem cells. Cultured iNPCs resemble closely primary human NPCs, generating nephron organoids with abundant distal convoluted tubule cells, which are not observed in published kidney organoids. The synthetic niche reprograms differentiated nephron cells into NPC state, recapitulating the plasticity of developing nephron in vivo. Scalability and ease of genome-editing in the cultured NPCs allow for genome-wide CRISPR screening, identi-fying novel genes associated with kidney development and disease. A rapid, efficient, and scala-ble organoid model for polycystic kidney disease was derived directly from genome-edited NPCs, and validated in drug screen. These technological platforms have broad applications to kidney development, disease, plasticity, and regeneration.

2024-03-14 | GSE251862 | GEO

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.

2024-03-21 | GSE224324 | GEO

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

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

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mRNA-Seq profiling nephron progenitor and stromal progenitor cells in mouse embryonic kidney

Project description:To characterize the expression profile of mouse nephron progenitors, we performed intracellular labeling of Six2 by antibody, followed by FACS and RNA-seq. To characterize the expression profile of mouse stromal progenitor cells, we isolated Tdt+ cells from Foxd1Cre;Tdt transgenic mice kidney by FACS followed by RNA-seq.

2018-02-14 | GSE102378 | GEO

Fate-mapping within human iPSC-derived kidney organoids reveals conserved mammalian nephron progenitor lineage relationships.

Project description:Early human kidney development is poorly documented due to tissue inaccessibility and a lack of genetic tractability. Here we combine reprogramming, CRISPR/Cas9 gene-editing and organoid technologies to study the nephron lineage in a human context. We confirm the presence of a SIX2+ population in early kidney organoids with a transcriptional profile akin to human fetal nephron progenitors. Using lineage-tracing analyses, we show that SIX2-expressing cells contribute to nephron formation but not to the putative collecting duct epithelium. Labeling of SIX2+ cells at various time-points during organoid differentiation revealed a markedly reduced capacity for these cells to contribute to nephron formation over time. This suggests human kidney organoids lack a true nephron progenitor niche, as the developing kidney does in vivo, capable of both self-renewal and ongoing nephrogeneis. Nonetheless, human iPSC-derived kidney tissue maintains previously identified lineage relationships, which supports the utility of in vitro organoid models for interrogating the molecular and cellular basis of early human development.

2019-03-12 | GSE119561 | GEO

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