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Related Concept Videos

Fixing Double-strand Breaks02:04

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 Breaks02:04

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 Cycle02:36

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 Cycle02:36

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 Recombination02:31

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...
Homologous Recombination02:31

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...

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Related Experiment Video

Updated: May 11, 2026

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
06:59

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter

Published on: March 31, 2022

From DNA damage to chromosome aberrations: joining the break.

M Durante1, J S Bedford, D J Chen

  • 1GSI Helmholtz Center for Heavy Ion Research, Darmstadt, Germany; Darmstadt University of Technology, Darmstadt, Germany.

Mutation Research
|May 28, 2013
PubMed
Summary

Radiation exposure causes DNA damage, leading to chromosomal aberrations. While some repair mechanisms are understood, the precise link between DNA double-strand break repair and the resulting chromosomal rearrangements remains unclear.

Keywords:
Chromosome aberrationsDNA double-strand breaksResection

More Related Videos

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

Published on: June 8, 2018

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells
13:10

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells

Published on: September 8, 2010

Related Experiment Videos

Last Updated: May 11, 2026

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter
06:59

Using Next Generation Sequencing to Identify Mutations Associated with Repair of a CAS9-induced Double Strand Break Near the CD4 Promoter

Published on: March 31, 2022

Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
08:31

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

Published on: June 8, 2018

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells
13:10

Analysis of DNA Double-strand Break (DSB) Repair in Mammalian Cells

Published on: September 8, 2010

Area of Science:

  • Cytogenetics
  • Molecular Biology
  • Radiation Biology

Background:

  • Radiation exposure induces DNA double-strand breaks (DSBs), a critical lesion.
  • The DNA damage response (DDR) pathways aim to repair DSBs, but misrepair can lead to chromosomal aberrations.
  • Despite advances, the precise relationship between DSB repair and the formation of visible chromosomal rearrangements is not fully understood.

Purpose of the Study:

  • To review and synthesize current understanding of the link between DNA double-strand break repair and radiation-induced chromosomal aberrations.
  • To discuss unresolved controversies and emerging concepts in the field.
  • To highlight the ongoing debate between molecular biologists and cytogeneticists.

Main Methods:

  • Literature review and synthesis of experimental findings.
  • Discussion of established and debated concepts in DNA repair and chromosomal aberration formation.
  • Summary of expert opinions from molecular biologists and cytogeneticists.

Main Results:

  • Key controversies regarding DSB induction dose-response, pairwise interaction, and lesion proximity have seen partial resolution.
  • The specific contributions of various DNA repair pathways, such as alternative end-joining, to aberration kinetics are still debated.
  • The definition of complex radiation-induced damaged sites, chemically or spatially, remains a subject of discussion.

Conclusions:

  • The precise molecular mechanisms by which DNA double-strand break repair influences the formation of chromosomal aberrations are still largely obscure.
  • Further research is needed to clarify the roles of different repair pathways and the nature of complex DNA damage.
  • Interdisciplinary dialogue between molecular biology and cytogenetics is crucial for advancing this field.