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Related Experiment Video

Updated: May 18, 2026

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney

Published on: April 22, 2011

A p53-Pax2 pathway in kidney development: implications for nephrogenesis.

Zubaida Saifudeen¹, Jiao Liu, Susana Dipp

¹Section of Pediatric Nephrology, Department of Pediatrics, Tulane University Health Sciences Center, New Orleans, Louisiana, United States of America. zubisaif@tulane.edu

|September 18, 2012

Summary

Reduced nephron number (renal hypoplasia) is linked to kidney disease. This study reveals that the p53 and Pax2 genes cooperate during kidney development to ensure proper nephron formation.

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Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions

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Published on: July 2, 2020

Area of Science:

Developmental Biology
Genetics
Nephrology

Background:

Congenital reduction in nephron number, or renal hypoplasia, is a risk factor for chronic kidney disease and hypertension.
While genes controlling nephrogenesis are known, the factors determining final nephron endowment remain unclear.

Purpose of the Study:

To investigate the potential cooperation between p53 and Pax2 in nephrogenesis.
To understand the molecular mechanisms underlying their interaction in kidney development.

Main Methods:

Utilized p53-deleted mouse models (germline and conditional) and Pax2 heterozygous mice.
Employed techniques including mRNA/protein analysis, ChIP-Seq, transient transfection assays, and p53 knockdown.
Bioinformatic analysis to identify co-regulated genes.

Main Results:

p53 deletion led to reduced Pax2 expression in nephron progenitors.
p53 directly binds to the Pax2 gene promoter and regulates its activity.
Reduced p53 function exacerbated renal hypoplasia in Pax2 heterozygous mice.
Identified co-regulated renal developmental genes.

Conclusions:

p53 and Pax2 genetically interact and cooperate in promoting nephrogenesis.
This cross-talk forms a transcriptional platform essential for establishing nephron endowment.
Findings provide insights into the genetic regulation of kidney development.