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Updated: Jun 21, 2026
14:57
Yeast As a Chassis for Developing Functional Assays to Study Human P53
Published on: August 4, 2019
Cell fate decision mediated by p53 pulses.
Xiao-Peng Zhang1, Feng Liu, Zhang Cheng
1National Laboratory of Solid State Microstructure and Department of Physics, Nanjing University, Nanjing 210093, China.
Summary
The tumor suppressor p53, activated by DNA damage, controls cell fate through pulsing. Low damage leads to survival via cell cycle arrest, while high damage triggers apoptosis, maintaining genomic integrity.
Area of Science:
- Cellular Biology
- Systems Biology
- Genetics
Background:
- The tumor suppressor p53 is vital for cellular stress response.
- Ionizing radiation (IR) induces pulsed p53 levels, but its role in cell fate is unclear.
Purpose of the Study:
- To explore the mechanism of cell fate decision based on p53 network dynamics.
- To understand how p53 pulses govern cell survival and death after DNA damage.
Main Methods:
- Development of an integrated four-module model for the p53 network.
- Numerical simulations to analyze network dynamics and cell fate determination.
Main Results:
- Activated ATM initiates p53 pulses, regulating target genes for cell fate.
- p53 promotes repair of minor DNA damage and suppresses severe damage repair.
- Cell fate depends on p53 pulse number: few pulses induce survival (p21), sustained pulses trigger apoptosis (p53AIP1).
- Stochasticity in DNA damage and repair influences cell fate variability.
Conclusions:
- p53 dynamics maintain genomic integrity by regulating DNA repair efficiency and fidelity.
- The number of p53 pulses dictates cell fate decisions in response to DNA damage extent.
- Findings align with experimental data, enhancing understanding of p53 network function.
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