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HUMAN FETAL KIDNEY ORGANOIDS MODEL EARLY NEPHROGENESIS AND NOTCH-DRIVEN CELL FATE [scRNA-seq]

ABSTRACT: HUMAN FETAL KIDNEY ORGANOIDS MODEL EARLY NEPHROGENESIS AND NOTCH-DRIVEN CELL FATE [scRNA-seq]

PROVIDER: PRJNA1279159 | ENA |

REPOSITORIES: ENA

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Human fetal kidney organoids model early human nephrogenesis and Notch-driven cell fate

Project description:Human fetal kidney organoids model early human nephrogenesis and Notch-driven cell fate

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Human fetal kidney organoids model early human nephrogenesis and notch-driven cell fate

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HUMAN FETAL KIDNEY ORGANOIDS MODEL EARLY NEPHROGENESIS AND NOTCH-DRIVEN CELL FATE [scRNA-Seq 2]

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HUMAN FETAL KIDNEY ORGANOIDS MODEL EARLY NEPHROGENESIS AND NOTCH-DRIVEN CELL FATE [scRNA-seq]

Project description:Pluripotent stem cell–derived kidney organoids (PSC-KOs) are widely used to model human kidney development and disease. However, organoids from human fetal kidney tissue (hFKOs), which could benchmark PSC-KOs, remain underdeveloped. Here, using a chemically defined serum-free medium, we established a prolonged culture protocol for hFKOs that self-organize into polarized renal epithelium, reinitiate from NCAM1+ progenitors, and recapitulate nephrogenic and ureteric bud lineages. Bulk transcriptomics, single-cell RNA sequencing, pseudotime analysis, and immunostaining revealed diverse cell populations, with a preserved epithelial progenitor pool and tubular differentiation axis—both more robust than in PSC-KOs. hFKOs were enriched for NOTCH signaling genes, enabling single-cell analysis of pharmacological NOTCH inhibition. This revealed a maturation block with increased nephron progenitors and a bias toward distal over early proximal tubule fates. We also identified a novel prominin-1–expressing cell state that evades NOTCH inhibition to generate both proximal and distal tubules. Overall, hFKOs provide a developmentally faithful model and offer critical insights into kidney morphogenesis, advancing the fields of stem cell biology and regenerative medicine.

2025-09-10 | GSE300166 | GEO

Human fetal kidney organoids model early human nephrogenesis and notch-driven cell fate

Project description:Pluripotent stem cell–derived kidney organoids (PSC-KOs) have been put forward as a preferred culture system in which to study human kidney development and disease. In contrast, the development of human fetal kidney tissue–derived organoids (hFKOs) that could serve as a benchmark for PSC-KOs has not advanced very far. Herein, utilizing a chemically defined serum-free medium, we established a long-term culture protocol for hFKOs that self-organize into polarized renal epithelium and faithfully recapitulate nephrogenic and ureteric bud cell lineages. Bulk transcriptomics, single-cell RNA sequencing, and pseudotime analysis along with immunostaining revealed diverse populations among hFKOs, with a preserved differentiation axis mostly at higher levels and to a greater extent than for PSC-KOs. Accordingly, compared to PSC-KOs, hFKOs were significantly enriched for the NOTCH signaling pathway genes, allowing single-cell analysis of changes following NOTCH inhibition. We observed a preferential increase of mature distal tubules at the expense of early proximal tubules and defined a new adaptive prominin 1–expressing (PROM1+, or CD133+) cell state that escapes NOTCH inhibition to generate proximal and distal tubules. Overall, the concomitant understanding of developmental processes using hFKOs is a key development for the fields of kidney stem cell biology and regenerative medicine.

2025-07-22 | GSE271315 | GEO

HUMAN FETAL KIDNEY ORGANOIDS MODEL EARLY NEPHROGENESIS AND NOTCH-DRIVEN CELL FATE [scRNA-Seq 2]

2025-09-10 | GSE300309 | GEO

Human fetal kidney organoids model early human nephrogenesis and Notch-driven cell fate.

Project description: Not available

| S-EPMC12402132 | biostudies-literature

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

Human fetal kidney organoids model early human nephrogenesis and Notch-driven cell fate

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-07-25 | GSE300015 | GEO

Human fetal kidney organoids model early human nephrogenesis and Notch-driven cell fate

Project description: Not available

| S-SCDT-10_1038-S44318-025-00504-2 | biostudies-other