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Related Concept Videos

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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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,...
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The DNA Replication Fork01:02

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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...
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Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
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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.
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Updated: Oct 25, 2025

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System
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Recombination-dependent replication: new perspectives from site-specific fork barriers.

Antony Carr1, Sarah Lambert2

  • 1Genome Damage and Stability Centre, School of Life Sciences, University of Sussex, Falmer, Sussex, BN1 9RQ, UK.

Current Opinion in Genetics & Development
|August 7, 2021
PubMed
Summary
This summary is machine-generated.

Replication stress (RS) is a natural process that can lead to genetic changes, especially in cancer. Understanding how cells restart stalled forks is key for cancer evolution and therapy.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Replication stress (RS) is inherent to cell growth and exacerbated by external factors and oncogene expression in cancer.
  • RS is a significant driver of genetic alterations, making tolerance mechanisms crucial for cancer evolution and targeted therapies.
  • Understanding RS is vital for developing novel cancer treatments.

Purpose of the Study:

  • To review recent findings on site-specific replication fork arrest systems.
  • To explore how these systems elucidate mechanisms of stalled fork restart and RS-dependent mutagenesis.
  • To highlight the strengths and limitations of yeast-based fork arrest models.

Main Methods:

  • Utilizing site-specific replication fork barriers in yeast models.
  • Analyzing mechanistic and spatial aspects of fork restart.
  • Correlating fork restart with replication stress-dependent mutagenesis.

Main Results:

  • Site-specific fork arrest systems offer unique insights into cellular responses to RS.
  • These systems have deepened the understanding of how arrested forks restart and their link to mutagenesis.
  • Recent data from yeast models provide valuable information on RS tolerance mechanisms.

Conclusions:

  • Site-specific fork arrest studies in yeast are powerful tools for dissecting RS response pathways.
  • This research advances our comprehension of cancer evolution and potential therapeutic strategies.
  • Further investigation into these mechanisms can reveal new avenues for cancer cell-specific interventions.