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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Related Experiment Video

Updated: Jun 3, 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 inhibits mRNA 3' processing through its interaction with the CstF/BARD1 complex.

F I Nazeer¹, E Devany, S Mohammed

¹Chemistry Department, Hunter College, City University of New York, New York, NY 10065, USA.

|March 9, 2011

Summary

The tumor suppressor p53 protein inhibits mRNA 3' cleavage during the DNA damage response. This novel function links RNA processing to the p53 network, impacting gene expression after UV exposure.

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Area of Science:

Molecular Biology
Cancer Research
Gene Regulation

Background:

The precise mechanisms of p53-mediated gene expression control after DNA damage remain unclear.
p53 is a critical tumor suppressor involved in cellular responses to DNA damage.

Purpose of the Study:

To elucidate the role of p53 in regulating mRNA 3' cleavage during the DNA damage response.
To investigate the interaction of p53 with factors involved in mRNA processing.

Main Methods:

Co-immunoprecipitation assays to detect protein complexes.
In vitro assays to assess p53's effect on mRNA 3' cleavage.
Analysis of p53 mutations and their impact on protein interactions and RNA processing.

Main Results:

p53 associates with BARD1 and CstF1, factors crucial for UV-induced inhibition of mRNA 3' cleavage.
p53 inhibits mRNA 3' cleavage in vitro, with its expression inversely correlated to cleavage levels.
A tumor-associated p53 mutation impairs interaction with BARD1/CstF and reduces UV-induced 3' processing inhibition.

Conclusions:

p53 possesses a novel inhibitory function in 3' RNA processing, adding complexity to the DNA damage response.
This function links RNA processing to the p53 network, influencing polyadenylation of specific genes.