Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mismatch Repair01:36

Mismatch Repair

Overview
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...
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...
Genome Copying Errors02:46

Genome Copying Errors

DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
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...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Reactivation of a TAL1 progenitor cell enhancer region by non-coding somatic variants in T-lineage acute lymphoblastic leukemia.

bioRxiv : the preprint server for biology·2026
Same author

The bacterial MRE11-RAD50 and DNA2-WRN homologs process replication forks at distinct and separate loci on the chromosome.

FEBS letters·2025
Same author

Topo IV is required to allow replisomes to converge and complete replication on the chromosome.

PLoS genetics·2025
Same author

High-throughput single-cell density measurements enable dynamic profiling of immune cell and drug response from patient samples.

Nature biomedical engineering·2025
Same author

The complex development of psoralen-interstrand crosslink resistance in Escherichia coli requires AcrR inactivation, retention of a marbox sequence, and one of three MarA, SoxS, or Rob global regulators.

Mutation research·2025
Same author

The complex development of psoralen-interstrand crosslink resistance in <i>Escherichia coli</i> requires AcrR inactivation, retention of a <i>marbox</i> sequence, and one of three MarA, SoxS, or Rob global regulators.

bioRxiv : the preprint server for biology·2024

Related Experiment Video

Updated: Jul 11, 2026

Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis
10:36

Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis

Published on: December 21, 2010

DNA damage-induced replication fork regression and processing in Escherichia coli.

Justin Courcelle1, Janet R Donaldson, Kin-Hoe Chow

  • 1Department of Biological Sciences, Box GY, Mississippi State University, Mississippi State, MS 39762, USA. jcourcelle@biology.msstate.edu

Science (New York, N.Y.)
|January 25, 2003
PubMed
Summary

DNA damage stalls replication forks, which can be reversed to allow repair. This fork regression, stabilized by RecA and RecF proteins in E. coli, is crucial for DNA repair and cell survival.

More Related Videos

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

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

Related Experiment Videos

Last Updated: Jul 11, 2026

Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis
10:36

Visualization of UV-induced Replication Intermediates in E. coli using Two-dimensional Agarose-gel Analysis

Published on: December 21, 2010

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

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
06:25

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

Published on: February 10, 2023

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA lesions blocking replication are a major cause of genetic instability and cell death.
  • Replication recovery after UV damage in E. coli depends on RecA and recF pathway proteins.

Purpose of the Study:

  • To investigate the mechanism of replication fork recovery after encountering DNA lesions.
  • To elucidate the role of RecA, RecF, RecQ, and RecJ proteins in this process.

Main Methods:

  • Utilized two-dimensional agarose gel electrophoresis to analyze replication fork dynamics in vivo.
  • Investigated the effects of mutations in recA, recF, recQ, and recJ genes on fork stability.

Main Results:

  • Replication-blocking DNA lesions induce a transient reversal (regression) of the replication fork in vivo.
  • The reversed fork intermediate is stabilized by RecA and RecF.
  • Absence of RecQ-RecJ helicase-nuclease leads to degradation of the reversed fork intermediate.

Conclusions:

  • Replication fork regression is a key mechanism for dealing with DNA lesions that impede DNA synthesis.
  • This process, mediated by proteins like RecA and RecF, allows access for DNA repair enzymes.
  • Successful repair enables the resumption of processive replication, ensuring cell viability.