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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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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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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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Overview of DNA Repair02:25

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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Updated: Jul 12, 2025

Author Spotlight: Characterizing DNA Replication of Pathogenic Repeats to Uncover Mechanisms of Replication Fork Stalling and Expansion
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Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.

Michal Irony-Tur Sinai1, Batsheva Kerem1

  • 1Department of Genetics, The Life Sciences Institute, The Hebrew University, Jerusalem, Israel.

Emerging Topics in Life Sciences
|October 25, 2023
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Summary

Common fragile sites (CFS) are genomic regions prone to instability during DNA replication. This study investigates molecular mechanisms of repeat instability at CFSs and proteins maintaining genome stability.

Keywords:
AT-dinucleotide rich sequencesaphidicolin-induced replication stresscommon fragile sitesgenomic instabilityrepeat instabilitysecondary structures

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Area of Science:

  • Genetics
  • Molecular Biology
  • Genomics

Background:

  • Common fragile sites (CFS) are genomic regions susceptible to chromosomal instability during DNA replication stress.
  • CFS instability is linked to copy number variants (CNVs) in cancer development.
  • CFS fragility involves replication timing, transcription, and genome organization.

Purpose of the Study:

  • To investigate the molecular mechanisms of repeat instability at CFSs.
  • To identify proteins involved in resolving secondary structures in repetitive sequences at CFSs.
  • To understand the role of these mechanisms in maintaining genome stability.

Main Methods:

  • Focus on molecular mechanisms of repeat instability at common fragile sites.
  • Analysis of proteins involved in resolving secondary structure impediments.
  • Examination of repetitive sequence elements crucial for genome stability.

Main Results:

  • CFS instability is associated with AT-rich repeats that form secondary structures impeding replication.
  • Specific proteins are crucial for resolving these secondary structures.
  • These mechanisms are essential for maintaining genome stability at CFSs.

Conclusions:

  • Repeat instability at CFSs is a significant factor in genomic instability.
  • Understanding the proteins involved in resolving secondary structures is key to maintaining genome stability.
  • Further research into these mechanisms can inform cancer development studies.