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

Histone Methylation Regulates Nephron Progenitor Cell Fate in Mice

Project description:We report the use of high-throughput sequencing of histone methylation ChIP to compare the H3K4me3 and H3K27me3 methylation states in sequential mouse nephron progenitor lineages Examination of 2 different histone modifications in 2 cell types.

2013-08-28 | E-GEOD-40742 | biostudies-arrayexpress

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

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

Reporter-based fate mapping in human kidney organoids confirms nephron lineage relationships and reveals synchronous nephron formation.

Project description:Nephron formation continues throughout kidney morphogenesis in both mice and humans. Lineage tracing studies in mice identified a self-renewing Six2-expressing nephron progenitor population able to give rise to the full complement of nephrons throughout kidney morphogenesis. To investigate the origin of nephrons within human pluripotent stem cell-derived kidney organoids, we performed a similar fate-mapping analysis of the SIX2-expressing lineage in induced pluripotent stem cell (iPSC)-derived kidney organoids to explore the feasibility of investigating lineage relationships in differentiating iPSCs in vitro Using CRISPR/Cas9 gene-edited lineage reporter lines, we show that SIX2-expressing cells give rise to nephron epithelial cell types but not to presumptive ureteric epithelium. The use of an inducible (CreERT2) line revealed a declining capacity for SIX2+ cells to contribute to nephron formation over time, but retention of nephron-forming capacity if provided an exogenous WNT signal. Hence, while human iPSC-derived kidney tissue appears to maintain lineage relationships previously identified in developing mouse kidney, unlike the developing kidney in vivo, kidney organoids lack a nephron progenitor niche capable of both self-renewal and ongoing nephrogenesis.

| S-EPMC6446205 | biostudies-literature

Histone Methylation Regulates Nephron Progenitor Cell Fate in Mice

2013-08-28 | GSE40742 | 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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data