Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA489582 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7791890_1.fastq.gz	Fastqsanger.gz
	SRR7791890_2.fastq.gz	Fastqsanger.gz
	SRR7791891_1.fastq.gz	Fastqsanger.gz
	SRR7791891_2.fastq.gz	Fastqsanger.gz
	SRR7791892_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

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

ChIP-seq of Smad3 and EZH2 binding sites in hiPSC and iPSC-derived Nephron Progenitors

Project description:Chromatin immunoprecipitation sequencing analysis of Smad3 and EZH2 binding sites in hIPSCs and iPSC-derived nephron progenitors.

2022-12-01 | E-MTAB-10910 | biostudies-arrayexpress

Gene expression profile of human iPSC-derived nephron progenitor cells

Project description:Gene expression profile of human iPSC-derived nephron progenitor cells

| PRJNA486586 | ENA

Gene expression profile of human iPSC-derived nephron progenitor cells

Project description:During development, nephron progenitor forming one million nephrons, a functional unit in the kidney. However, nephron progenitor ceases before birth in human when they terminally differentiated to the nephron. Our lab established the method for induction of nephron progenitors from mouse Embryonic Stem (ES) cells and/or human induced Pluripotent Stem Cells (iPSCs) (Taguchi et al., Cell Stem Cell. 2014, 2017). For application of induced nephron progenitors to regenerative medicine, a large number of cells are required such as disease modeling and drug screening. To selectively propagate human iPS-derived nephron progenitors in vitro in an undifferentiated state, we developed SIX2-GFP iPS line and optimized culture condition of induced nephron progenitors by modifying our previously developed condition (Tanigawa et al., Cell Rep. 2016). To understand how whole gene expression profiles of human iPS-derived nephron progenitor cells are changed during culture, we isolated nephron progenitor cells by FACS and cultured in our defined culture condition. Purified RNAs from cultured cells at day 7 or un-cultured nephron progenitor cells were analyzed by RNA-seq.

2019-08-01 | GSE118729 | GEO

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.

2017-03-11 | GSE79137 | GEO

Nephron endowment

Project description:Nephron endowment

| PRJNA298245 | ENA

Revisiting the Role of Notch in Nephron Segmentation Confirms A Role for Proximal Fate Selection During Mouse and Human Nephrogenesis

Project description:Notch signaling promotes maturation of nephron epithelia, but its proposed contribution to nephron segmentation into proximal and distal domains has been called into doubt. We leveraged single cell and bulk RNA-seq, quantitative immunofluorescent lineage/fate tracing, and genetically modified human iPSC to revisit this question in developing mouse kidneys and human kidney organoids. We confirmed that Notch signaling is needed for maturation of all nephron lineages, and thus mature lineage markers fail to detect a fate bias. By contrast, early markers identified a distal fate bias in cells lacking Notch2, and a concomitant increase in early proximal and podocyte fates in cells expressing hyperactive Notch1 was observed. Orthogonal support for a conserved role for Notch signaling in the distal/proximal axis segmentation is provided by the demonstration that Nicastrin-deficient hiPSCs-derived organoids differentiate into TFA2B+ distal tubule and CDH1 connecting segment progenitors, but not into HNF4A+ or LTL+ proximal progenitors.

2022-05-04 | GSE201938 | GEO

Transcriptional response of cap mesenchyme (undifferentiated nephron progenitors) to Wnt activation

Project description:During mammalian kidney development, mesenchymal nephron progenitors (cap mesenchyme) differentiate into the epithelial cells that go on to form the nephron. Although differentiation of nephron progenitors is triggered by activation of Wnt/b-catenin signaling, constitutive activation of Wnt/b-catenin signaling blocks epithelialization of nephron progenitors. Full epithelialization of nephron progenitors requires transient activation of Wnt/b-catenin signaling. We performed transcriptional profiling of nephron progenitors responding to constitutive or transient activation of Wnt/b-catenin signaling. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. Cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing either 4uM BIO or the equal volume of DMSO for 24hrs or 48hrs.

2012-09-11 | E-GEOD-39583 | biostudies-arrayexpress

Intrinsic age-dependent changes and cell-cell contacts regulate nephron progenitor lifespan

Project description:Purpose: To use single-cell RNA-Seq analysis of nephron progenitors in order to determine transcrptional differences as nephron progenitors age. Methods: Using a combination of FACS sorting and a Fluidigm Single-cell auto-prep system, we generated high-throughput RNA-SEQ data of nephron progenitors during development Results: Single cells transcriptome profiling of nephron progenitors revealed progressive age-dependent changes with heterogeneity increasing in older populations. 96-single cell transcriptomes were determined from nephron progenitors of e14.5, e18.5 and P0 using Cited1GFP transgenic animals

2015-12-23 | E-GEOD-66202 | biostudies-arrayexpress

ChIP-seq of Smad3 and EZH2 binding sites in hiPSC and iPSC-derived Nephron Progenitors

Project description:ChIP-seq of Smad3 and EZH2 binding sites in hiPSC and iPSC-derived Nephron Progenitors

| PRJEB47435 | ENA