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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.
Chemically...

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.
Chemically...

Fixing Double-strand Breaks

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...

Fixing Double-strand Breaks

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...

Nucleotide Excision Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...

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Related Experiment Video

Updated: Jun 22, 2026

Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome

Electrophoretic Analysis of Replication Through Structure-Prone DNA Repeats Within the SV40-Based Human Episome

Published on: September 13, 2024

Structure-dependent DNA damage and repair in a trinucleotide repeat sequence.

Daniel A Jarem¹, Nicole R Wilson, Sarah Delaney

¹Department of Chemistry, Brown University, Providence, Rhode Island 02912, USA.

|June 17, 2009

Summary

Triplet repeat sequences in DNA can form hairpin structures that are prone to damage. The enzyme human OGG1 repairs this damage inefficiently, potentially explaining trinucleotide repeat expansion in neurological disorders.

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

Published on: August 21, 2021

Area of Science:

Genetics
Molecular Biology
Biochemistry

Background:

Triplet repeat sequences (e.g., CAG/CTG) are implicated in neurological disorders.
Non-B DNA conformations are proposed to play a role in repeat expansion.
The base excision repair enzyme 7,8-dihydro-8-oxoguanine glycosylase (OGG1) is linked to repeat expansion.

Purpose of the Study:

To investigate the susceptibility of non-B DNA conformations to DNA damage.
To determine the efficiency of human OGG1 in repairing damaged hairpin DNA structures.
To explore the role of DNA damage and repair in trinucleotide repeat expansion.

Main Methods:

Comparative analysis of DNA damage in hairpin versus duplex (CAG)(10) sequences.
Assessment of peroxynitrite modification of guanine in hairpin structures.
Enzymatic assays measuring the excision of 8-oxoguanine by human OGG1 from hairpin and duplex substrates.

Main Results:

The hairpin conformation of (CAG)(10) is more susceptible to DNA damage than its duplex form.
A specific guanine in the hairpin loop is a hot spot for peroxynitrite modification.
Human OGG1 excises 8-oxoguanine from hairpin loops, but approximately 700-fold less efficiently than from duplex DNA.

Conclusions:

DNA damage preferentially occurs in the hairpin loop of triplet repeat sequences.
Reduced repair efficiency of damaged hairpin structures by hOGG1 may contribute to repeat expansion.
Structure-dependent DNA damage and repair patterns offer insights into the OGG1-dependent mechanism of trinucleotide repeat expansion.