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Overview of DNA Repair

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Overview of DNA Repair

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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: Nov 9, 2025

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

It takes three to the DNA damage response tango.

Sapir Schlam-Babayov¹, Yael Ziv¹, Yosef Shiloh¹

¹The David and Inez Myers Laboratory of Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Tel Aviv University School of Medicine, Tel Aviv, Israel.

Molecular & Cellular Oncology

|April 16, 2021

Summary

The DNA damage response relies on three key kinases. ATR and DNA-PK compensate for ATM

Keywords:

ATM Ataxia-telangiectasia DNA damage response PIKKs phosphoproteomic

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Area of Science:

Molecular Biology
Cellular Biology
Genetics

Background:

The DNA damage response (DDR) is crucial for maintaining genomic stability.
DNA double-strand breaks (DSBs) trigger a complex signaling network.
Three PI3-kinase-related protein kinases (PIKKs) — ATM, ATR, and DNA-PK — are central regulators of the DDR.

Purpose of the Study:

To elucidate the relative contributions of ATM, ATR, and DNA-PK in coordinating the DDR.
To investigate the compensatory mechanisms involving ATR and DNA-PK in the absence of ATM, as observed in ataxia-telangiectasia (A-T).

Main Methods:

Phosphoproteomic analysis was employed to quantify the activity and targets of PIKKs.
Comparative analysis was performed in the presence and absence of ATM function.

Main Results:

Phosphoproteomic data revealed the distinct roles and relative importance of ATM, ATR, and DNA-PK in the DDR network.
The study demonstrated that ATR and DNA-PK can compensate for the loss of ATM function in cells from A-T patients.

Conclusions:

ATM, ATR, and DNA-PK play coordinated yet distinct roles in the DDR.
ATR and DNA-PK provide functional redundancy, compensating for ATM deficiency in A-T, thereby highlighting the robustness of the DDR network.