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DNA Damage Can Stall the Cell Cycle

DNA Damage Can Stall the Cell Cycle

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...

DNA Damage can Stall the Cell Cycle

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Related Experiment Video

Updated: May 26, 2026

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

DNA damage signals through differentially modified E2F1 molecules to induce apoptosis.

Jasmyne Carnevale¹, Oliva Palander, Laurie A Seifried

¹London Regional Cancer Program, London, Ontario, Canada.

Molecular and Cellular Biology

|December 21, 2011

Summary

DNA damage triggers distinct forms of E2F1 (transcription factor E2F1) with specific modifications. These forms, bound or free from pRB, are crucial for activating apoptosis, revealing a new role for E2F1 in cell death pathways.

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

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Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

Area of Science:

Cellular Biology
Molecular Biology
Genetics

Background:

E2F transcription factors regulate cell proliferation and apoptosis.
DNA double-strand breaks can induce cell cycle arrest or apoptosis.
pRB activation by DNA damage sequesters E2Fs, but E2F1 is also activated for proapoptotic transcription.

Purpose of the Study:

Investigate the regulation of E2F1 interaction with pRB following DNA damage.
Elucidate the mechanisms behind the paradoxical control of E2F transcription.

Main Methods:

Studied posttranslational modifications of E2F1.
Utilized chromatin immunoprecipitation to analyze E2F1 binding to gene promoters.
Examined the role of distinct E2F1 forms in apoptosis induction.

Main Results:

DNA damage generates multiple E2F1 forms with mutually exclusive posttranslational modifications.
E2F1 phospho-serine 364 is pRB-bound, while other modifications create a pRB-free E2F1.
Both E2F1 forms are essential for TA-p73 activation and maximal apoptosis induction.
Distinct E2F1 populations operate in parallel to activate proapoptotic genes.

Conclusions:

DNA damage signaling creates distinct E2F1 populations with specific modifications.
These distinct E2F1 forms play parallel roles in activating proapoptotic gene transcription.
E2F1 and pRB engage in apoptosis-inducing functions distinct from cell cycle control.