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Updated: Jun 17, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

p53 and stem cells: new developments and new concerns.

Tongbiao Zhao¹, Yang Xu

¹Section of Molecular Biology, Division of Biological Sciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0322, USA.

Trends in Cell Biology

|January 12, 2010

Summary

This summary is machine-generated.

The tumor suppressor p53 prevents genetic mutations and suppresses pluripotency. Its inactivation is crucial for induced pluripotent stem cells (iPSCs), raising concerns about iPSC genomic stability and tumorigenecity.

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Area of Science:

Molecular Biology
Cancer Research
Stem Cell Biology

Background:

The tumor suppressor p53 acts as the guardian of the genome, preventing genetic mutations by inducing cell cycle arrest, apoptosis, or senescence in response to cellular stress.
Emerging research highlights p53's role in inhibiting pluripotency and cellular dedifferentiation processes.

Purpose of the Study:

To investigate the role of p53 as a barrier to pluripotency and cellular dedifferentiation.
To understand the implications of p53's function in the reprogramming of somatic cells into induced pluripotent stem cells (iPSCs).

Main Methods:

Review of recent studies on p53 function in embryonic stem cells and somatic cell reprogramming.
Analysis of the impact of p53 inactivation on the generation and characteristics of iPSCs.

Main Results:

p53 actively suppresses the self-renewal of embryonic stem cells following DNA damage.
p53 inhibits the reprogramming of somatic cells into induced pluripotent stem cells (iPSCs).
Inactivation of the p53 pathway appears necessary for successful cellular reprogramming.

Conclusions:

The findings suggest that p53 acts as a significant barrier to achieving pluripotency and dedifferentiation.
The necessity of p53 inactivation for reprogramming raises critical questions regarding the genomic stability and tumorigenic potential of iPSCs and their derivatives.
Further elucidation of p53's role may uncover mechanisms linking tumor suppression and aging.