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Related Concept Videos

The DNA Replication Fork01:02

The DNA Replication Fork

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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 Damage can Stall the Cell Cycle02:37

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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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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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DNA Damage Can Stall the Cell Cycle02:37

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Overview of DNA Repair02:25

Overview of DNA Repair

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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.
Chemically...
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S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
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Related Experiment Video

Updated: Jul 9, 2025

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

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Cellular Responses to Widespread DNA Replication Stress.

Jac A Nickoloff1, Aruna S Jaiswal2, Neelam Sharma1

  • 1Department of Environmental and Radiological Health Sciences, Colorado State University, Ft. Collins, CO 80523, USA.

International Journal of Molecular Sciences
|December 9, 2023
PubMed
Summary

DNA replication stress, caused by damage or difficult sequences, triggers cell responses to maintain genome stability. Nucleases are key to repairing stressed replication forks, offering cancer treatment insights.

Keywords:
DNA damageDNA damage responseDNA double-strand breaksgenome instabilityoxidative DNA damagereplication stressstructure-specific nucleases

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Replicative DNA polymerases encounter various DNA damages, leading to replication stress that compromises genome stability.
  • Replication stress arises from DNA damage, nucleotide pool imbalances, polymerase inhibitors, and challenging DNA structures like G-quadruplexes.
  • Cellular responses to replication stress involve cell cycle arrest, fork collapse, DNA repair, and apoptosis, with specific nucleases playing critical roles.

Purpose of the Study:

  • To review cellular responses to widespread replication stress, including damage, polymerase inhibition, nucleotide depletion, and R-loops.
  • To highlight the role of nucleases in resolving stalled replication forks and maintaining genome integrity.
  • To discuss the implications of replication stress responses for cancer biology and therapeutic strategies.

Main Methods:

  • Literature review of cellular responses to replication stress.
  • Focus on the functions of various nucleases (e.g., MUS81, EEPD1, TATDN2) in DNA repair and replication restart.
  • Discussion of oncogenic stress in cancer and its link to replication stress response pathways.

Main Results:

  • Nucleases like EEPD1 and TATDN2 are crucial for restarting stressed replication forks and mitigating specific types of replication stress.
  • Dysregulation of replication stress responses in cancer cells contributes to genome instability and cancer progression.
  • Several nucleases cleave branched DNA structures at stressed forks, facilitating repair and restart.

Conclusions:

  • Cellular responses to replication stress are vital for genome stability, involving a complex network of repair pathways.
  • Insights into replication stress mechanisms, particularly the roles of nucleases, offer potential for novel cancer therapies targeting synthetic lethality.
  • Understanding oncogenic stress and its interaction with replication stress pathways is crucial for cancer treatment development.