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Related Concept Videos

Restarting Stalled Replication Forks02:37

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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 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...
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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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Updated: Feb 27, 2026

Inducing a Site Specific Replication Blockage in E. coli Using a Fluorescent Repressor Operator System
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Template-switching during replication fork repair in bacteria.

Susan T Lovett1

  • 1Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, MA, 2454-9110, USA.

DNA Repair
|June 24, 2017
PubMed
Summary
This summary is machine-generated.

Replication forks can stall due to DNA damage or other obstacles, leading to gaps that are repaired by template-switching. This process can cause genetic instability and mutations.

Keywords:
Copy number variationDNA replicationGenetic recombinationMutagenesisPostreplication repairQuasipalindrome

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Replication forks face challenges like DNA lesions, secondary structures, and protein impediments.
  • Bacterial studies suggest these challenges can create single-strand DNA gaps.
  • These gaps are repaired via homologous recombination, translesion synthesis, or template-switching.

Purpose of the Study:

  • To review template-switching repair pathways.
  • To explore mechanisms deduced from biochemical and genetic studies.
  • To discuss the role of template-switching in genetic instability.

Main Methods:

  • Review of existing literature.
  • Analysis of biochemical studies.
  • Analysis of genetic studies.

Main Results:

  • Template-switching is a key repair mechanism for replication fork stress.
  • Biochemical and genetic studies have elucidated its mechanisms.
  • Template-switching contributes to genetic instability, mutational hotspots, and rearrangements.

Conclusions:

  • Template-switching pathways are crucial for repairing damaged replication forks.
  • Understanding these pathways reveals mechanisms underlying genetic instability.
  • Replication fork damage can trigger template-switching repair.