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p53-dependent cell cycle control: response to genotoxic stress.

D Schwartz¹, V Rotter

¹Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.

Seminars in Cancer Biology

|April 2, 1999

Summary

The p53 protein acts as the guardian of the genome by controlling cell cycle checkpoints and promoting apoptosis in response to DNA damage. This review focuses on p53

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Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

The p53 protein is a critical regulator of cellular responses to genotoxic stress.
Its functions are essential for maintaining genomic stability and preventing cancer.
p53 acts as a tumor suppressor by orchestrating cell cycle arrest and apoptosis.

Purpose of the Study:

To review the molecular pathways through which p53 controls the cell cycle.
To emphasize the significance of p53-mediated checkpoint responses in its tumor suppressor role.
To discuss findings from various in vivo mouse models relevant to p53 function.

Main Methods:

Review of existing literature on p53 molecular pathways.
Analysis of data from p53 knockout and transgenic mouse models.
Examination of studies involving knockout mice for genes upstream or downstream of p53.

Main Results:

p53 mediates cell cycle arrest at G1/S, G2, and spindle checkpoints in response to DNA damage.
Low DNA damage allows for repair during p53-induced cell cycle delays.
High or irreparable DNA damage triggers p53-dependent apoptosis.
In vivo mouse models have elucidated the critical role of p53 in tumor suppression.

Conclusions:

p53's role as the 'guardian of the genome' is substantiated by its control over cell cycle checkpoints and apoptosis.
Understanding p53 pathways is crucial for comprehending its tumor suppressor function.
In vivo studies, particularly using mouse models, provide valuable insights into p53's in vivo functions and relevance to cancer.

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