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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...

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 Replisome

The Replisome

DNA replication is carried out by a large complex of proteins that act in a coordinated matter to achieve high-fidelity DNA replication. Together this complex is known as the DNA replication machinery or the replisome.
The synthesis of the leading and lagging strands is a highly coordinated process. To explain this, the “Trombone model” was proposed by Bruce Alberts in 1980. The DNA loop formation starts when a primer is synthesized on the parent lagging strand. The loop grows with the...

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Related Experiment Video

Updated: Jun 4, 2026

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

A Blm-Recql5 partnership in replication stress response.

Xincheng Lu¹, Hua Lou, Guangbin Luo

¹Institute of Genomic Medicine, Wenzhou Medical College, Wenzhou 325027, China.

Journal of Molecular Cell Biology

|February 1, 2011

Summary

DNA repair deficiencies can cause cancer. This study reveals a partnership between Blm and Recql5 helicases that protects against replication stress, offering insights for cancer treatment.

Area of Science:

Molecular Biology
Genetics
Cancer Research

Background:

DNA damage response and repair are crucial for preventing genome instability and cancer.
Replication stress is a common feature in human cancers, leading to instability and cell death.
Mammalian RecQ helicases, including Blm and Recql5, play vital roles in DNA repair.

Purpose of the Study:

To review the partnership between Blm and Recql5 helicases in DNA replication and cell survival.
To investigate the role of Recql5 in suppressing replication fork collapse under replication stress.
To discuss the implications of these findings for anticancer therapies.

Main Methods:

Genetic knockout studies of Blm and Recql5 in mammalian cells.
Analysis of DNA replication fork dynamics under replication stress.

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Visualization of Replisome Encounters with an Antigen Tagged Blocking Lesion

Visualization of Replisome Encounters with an Antigen Tagged Blocking Lesion

Published on: July 27, 2021

Related Experiment Videos

Last Updated: Jun 4, 2026

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

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

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

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Visualization of Replisome Encounters with an Antigen Tagged Blocking Lesion

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Review of existing literature on RecQ helicases and camptothecin treatment.

Main Results:

Blm and Recql5 exhibit a unique partnership in managing replication stress.
A novel Recql5-dependent mechanism suppresses replication fork collapse.
This partnership promotes DNA replication, cell survival, and suppresses genome instability.

Conclusions:

The Blm-Recql5 partnership is essential for coping with replication stress.
Understanding this mechanism may lead to improved anticancer treatments using camptothecin derivatives.
Targeting these helicases could enhance the efficacy of existing cancer therapies.