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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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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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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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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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Related Experiment Video

Updated: Jun 30, 2025

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication
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RPA and Rad27 limit templated and inverted insertions at DNA breaks.

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    Templated insertions at DNA double-strand breaks (DSBs) are common in cancer. A hybrid mechanism involving DNA polymerase delta and nonhomologous end joining, exacerbated by RPA deficiency, drives these events.

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    Area of Science:

    • Molecular Biology
    • Genetics
    • Cancer Research

    Background:

    • Formation of templated insertions at DNA double-strand breaks (DSBs) is frequent in cancer cells, yet the underlying mechanisms and enzymes remain poorly understood.
    • Understanding these processes is crucial for deciphering cancer genome instability and developing targeted therapies.

    Approach:

    • Investigated templated insertions at DSBs in yeast using amplicon sequencing of a repaired locus.
    • Characterized the size, structure, and formation mechanism of these insertions, identifying the roles of specific enzymes and DNA repair pathways.

    Key Points:

    • Identified very short (∼5-34 bp) templated inverted duplications at DSBs, formed via a foldback mechanism using microhomologies.
    • Proposed a hybrid DNA repair mechanism involving Polδ-mediated synthesis and nonhomologous end joining (NHEJ).
    • Observed increased templated insertions in mutants with deficient RPA or extensive DNA resection (sgs1Δ exo1Δ), and in rad27Δ mutants, often originating from fragile genomic regions.

    Conclusions:

    • A shortage of Replication Protein A (RPA), common in cancer cells, may stimulate the formation of templated insertions.
    • The findings shed light on the complex DNA repair pathways contributing to genomic alterations in cancer.