Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Restarting Stalled Replication Forks

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...

Restarting Stalled Replication Forks

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...

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...

The DNA Replication Fork

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork. Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication forks, one in...

The DNA Replication Fork

The DNA Replication Fork

An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork. Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication forks, one in...

Genome Copying Errors

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.

You might also read

Related Articles

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

Sort by

Same author

Targeting p130Cas- and microtubule-dependent MYC regulation sensitizes pancreatic cancer to ERK MAPK inhibition.

Cell reports·2026

Same author

Time-resolved functional genomics using deep learning reveals global hierarchical control of autophagy.

Nature cell biology·2026

Same author

DNA mismatch repair mediated by Mlh1-Pms1 endonuclease-catalyzed mispair excision.

Proceedings of the National Academy of Sciences of the United States of America·2025

Same author

Modulating NLRP3 splicing with antisense oligonucleotides to control pathological inflammation.

Nucleic acids research·2025

Same author

Frataxin Traps Low Abundance Quaternary Structure to Stimulate Human Fe-S Cluster Biosynthesis.

Biochemistry·2025

Same author

The <i>Saccharomyces cerevisiae</i> cell lysis mutant <i>cly8</i> is a temperature-sensitive allele of <i>ESP1</i>.

bioRxiv : the preprint server for biology·2024

Search research articles

Related Experiment Video

Updated: Jun 13, 2026

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

Post-replication repair suppresses duplication-mediated genome instability.

Christopher D Putnam¹, Tikvah K Hayes, Richard D Kolodner

¹Ludwig Institute for Cancer Research, University of California San Diego School of Medicine, La Jolla, California, United States of America.

|May 14, 2010

Summary

This summary is machine-generated.

The RAD6- and RAD18-dependent post-replication repair (PRR) pathway, along with error-free PRR, suppresses duplication-mediated gross chromosomal rearrangements (GCRs). This pathway works with the replication stress checkpoint to prevent GCRs via homologous recombination (HR).

More Related Videos

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

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

Published on: February 10, 2023

Related Experiment Videos

Last Updated: Jun 13, 2026

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay

Published on: February 3, 2022

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

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

Published on: February 10, 2023

Area of Science:

Molecular Biology
Genetics
DNA Repair Mechanisms

Background:

RAD6 is known to suppress duplication-mediated gross chromosomal rearrangements (GCRs) but not single-copy sequence mediated GCRs.
Understanding the mechanisms that prevent GCRs is crucial for genomic stability.

Purpose of the Study:

To investigate the concerted action of post-replication repair (PRR) pathways and the replication stress checkpoint in suppressing duplication-mediated GCRs.
To elucidate the specific roles of key proteins like RAD6, RAD18, and RAD5 in preventing chromosomal instability.

Main Methods:

Utilized genetic epistasis analysis to determine the order of function for helicases SRS2, SGS1, and HCS1 in relation to RAD5.
Investigated the requirement of RAD5 helicase activity and PCNA modification at Lys164 for preventing GCRs.
Examined the interaction between PRR pathways and the replication stress checkpoint.

Main Results:

The RAD6/RAD18-dependent PRR and the RAD5/MMS2/UBC13-dependent error-free PRR branch function with the replication stress checkpoint to suppress duplication-mediated GCRs via homologous recombination (HR).
RAD5 helicase activity, but not its RING finger, is essential for preventing these GCRs, dependent on PCNA modification at Lys164.
SRS2 and HCS1 helicases act upstream of RAD5, while SGS1 functions downstream, potentially resolving DNA structures generated by RAD5.

Conclusions:

PRR pathways act in concert with the replication stress checkpoint to prevent replication damage from escalating into double-strand breaks (DSBs).
These pathways play a critical role in regulating homologous recombination (HR) activity on DSBs, thereby maintaining genomic integrity.
The findings provide a detailed mechanistic insight into the suppression of duplication-mediated GCRs.