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Related Concept Videos

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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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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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Actin Polymerization01:42

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Actin polymerization occurs through the head-to-tail association of binding sites on monomeric actin or G-actin to form filamentous or F-actin. The polymerization can be divided into three phases ̶  nucleation, elongation, and steady-state phase.
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The Replisome03:01

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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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Actin Filament Depolymerization01:19

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Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
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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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Updated: Aug 5, 2025

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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Replication fork plasticity upon replication stress requires rapid nuclear actin polymerization.

Maria Dilia Palumbieri, Chiara Merigliano, Daniel González Acosta

    Biorxiv : the Preprint Server for Biology
    |March 30, 2023
    PubMed
    Summary
    This summary is machine-generated.

    Nuclear actin filaments orchestrate DNA replication fork plasticity, enabling cells to respond rapidly to genotoxic stress by slowing and reversing forks. This actin-mediated process is crucial for maintaining genomic stability.

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    Area of Science:

    • Cellular Biology
    • Molecular Biology
    • Genomics

    Background:

    • Cells possess mechanisms to manage replication stress, including slowing and reversing replication forks.
    • The role of nuclear organization, specifically nuclear actin, in replication fork plasticity remains largely unexplored.

    Approach:

    • Utilized nuclear actin probes in live and fixed cells to visualize actin dynamics during S phase and in response to genotoxic treatments.
    • Investigated the impact of inhibiting nuclear actin polymerization on replication fork progression and associated protein recruitment.
    • Assessed the consequences of impaired fork plasticity on DNA synthesis, chromosomal stability, and cellular resistance to replication stress.

    Key Points:

    • Nuclear actin filaments rapidly increase in number and thickness upon genotoxic stress, interacting with replication factories.
    • Impairment of nuclear actin polymerization prevents active replication fork slowing and reversal.
    • Defective fork plasticity leads to reduced RAD51 and SMARCAL1 recruitment and increased PRIMPOL access to chromatin.
    • Unrestrained DNA synthesis due to impaired fork plasticity correlates with increased chromosomal instability and reduced resistance to replication stress.

    Conclusions:

    • Nuclear F-actin plays a critical role in orchestrating replication fork plasticity.
    • Nuclear actin is a key determinant in the rapid cellular response to genotoxic stress, maintaining genomic integrity.