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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...

Base Excision Repair

Base Excision Repair

One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...

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...

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...

Homologous Recombination

Homologous Recombination

The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...

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...

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Related Experiment Video

Updated: Jul 10, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

Effect of DNA damage on a BRCA1 complex.

F Wu-Baer¹, R Baer

¹Institute of Cancer Genetics and Department of Pathology, Columbia University College of Physicians and Surgeons, 1150 St Nicholas Avenue, New York, New York 10032, USA.

|November 2, 2001

Summary

The BRCA1-CtIP complex remains stable after DNA damage, contrary to previous findings. Phosphorylation of CtIP by ATM kinase does not disrupt this interaction, impacting DNA damage response gene transcription.

Area of Science:

Molecular Biology
Cellular Biology
Genetics

Background:

The tumor suppressor BRCA1 protein interacts with CtIP, a substrate of ATM kinase.
Previous studies suggested that genotoxic stress disrupts the BRCA1-CtIP interaction via CtIP phosphorylation.

Purpose of the Study:

To investigate the effect of ionizing radiation and ATM kinase-mediated phosphorylation on the BRCA1-CtIP complex stability.
To determine if BRCA1-CtIP complex disruption mediates the transcription of DNA-damage-response genes.

Main Methods:

Investigated the stability of the BRCA1-CtIP complex in irradiated cells.
Analyzed the interaction of phosphorylated CtIP isoforms with BRCA1 in vivo.
Mapped the BRCA1-binding domain of CtIP relative to ATM phosphorylation sites.

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Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

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Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

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Last Updated: Jul 10, 2026

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1

Published on: February 17, 2011

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy

Published on: June 8, 2018

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Main Results:

The BRCA1-CtIP complex remains stable in cells exposed to ionizing radiation.
Phosphorylation of CtIP by ATM kinase does not prevent its in vivo interaction with BRCA1.
The BRCA1-binding domain of CtIP is distinct from ATM phosphorylation sites.

Conclusions:

Disruption of the BRCA1-CtIP complex is not the mechanism by which DNA-damage-response genes are induced after genotoxic stress.
The findings challenge the model proposed by Li et al. regarding BRCA1-CtIP complex dissociation and gene regulation.