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Related Concept Videos

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...
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...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
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...

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Related Experiment Video

Updated: Jun 20, 2026

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae
07:55

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae

Published on: September 11, 2022

Checkpoint signaling from a single DNA interstrand crosslink.

Merav Ben-Yehoyada1, Lily C Wang, Ivan D Kozekov

  • 1Institute for Cancer Genetics, Department of Genetics and Development, Columbia University, New York, NY 10032, USA.

Molecular Cell
|September 15, 2009
PubMed
Summary

DNA interstrand crosslinks (ICLs) are toxic DNA lesions. This study reveals ICLs trigger checkpoints independently of replication and details their error-free repair, offering insights into chemotherapy sensitivity.

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

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Related Experiment Videos

Last Updated: Jun 20, 2026

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae
07:55

Detection of Homologous Recombination Intermediates via Proximity Ligation and Quantitative PCR in Saccharomyces cerevisiae

Published on: September 11, 2022

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

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

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA interstrand crosslinks (ICLs) are highly toxic DNA lesions.
  • Chemotherapeutic agents like mitomycin C and cisplatin induce ICLs, hindering DNA replication and transcription.
  • Previous studies on ICL signaling and repair were complicated by additional DNA damage signaling.

Purpose of the Study:

  • To monitor the sensing, signaling, and repair of a single site-specific ICL.
  • To investigate ICL-induced checkpoint activation independent of DNA replication.
  • To elucidate the mechanisms of ICL repair and their relation to cellular sensitivity.

Main Methods:

  • Utilized cell-free extracts from Xenopus eggs and mammalian cells.
  • Monitored the response to a single site-specific ICL.
  • Investigated the Fanconi anemia pathway's role in ICL signaling.

Main Results:

  • ICLs trigger checkpoint responses independently of DNA replication initiation and polymerase-helicase uncoupling.
  • The Fanconi anemia pathway acts upstream of RPA-ATR-Chk1 signaling.
  • ICLs are repaired via extensive, error-free DNA synthesis through both origin-dependent and independent pathways.

Conclusions:

  • Cellular sensitivity to crosslinking agents stems from defects in both checkpoint activation and DNA repair.
  • The Fanconi anemia pathway is crucial for initiating the ICL damage signal.
  • Error-free DNA synthesis is a key component of ICL repair.