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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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Duplication of Chromatin Structure02:05

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The process of chromosome duplication during cell division requires genome-wide disruption and re-assembly of chromatin. The chromatin structure must be accurately inherited, reassembled, and maintained in the daughter cells to ensure lineage propagation.
The basic unit of the chromatin is the nucleosome, consisting of DNA wrapped around octameric histone proteins and short stretches of linker DNA separating individual nucleosomes. The histone proteins within the nucleosome have their...
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Chromosome Replication02:31

Chromosome Replication

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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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Replication in Eukaryotes01:29

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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
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Chromosome Structure02:40

Chromosome Structure

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A functional eukaryotic chromosome must contain three elements: a centromere, telomeres, and numerous origins of 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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Related Experiment Video

Updated: Oct 22, 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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Replication stress: from chromatin to immunity and beyond.

Yea-Lih Lin1, Philippe Pasero1

  • 1Institut de Génétique Humaine, CNRS, Université de Montpellier, Equipe Labellisée Ligue Contre le Cancer, 34396 Montpellier, France.

Current Opinion in Genetics & Development
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Replication stress (RS) in cancer cells causes genomic instability. Understanding RS, its causes, and its link to immunity offers new cancer therapy strategies.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Replication stress (RS) is a key feature of cancer cells, contributing to genomic instability.
  • RS arises when DNA replication forks face obstacles, leading to stalling.
  • Checkpoint kinases and chromatin remodelers are crucial for managing stalled forks and facilitating repair.

Purpose of the Study:

  • To review recent findings on the causes and consequences of replication stress.
  • To highlight the impact of endogenous replication impediments on fork velocity.
  • To explore the connection between stalled forks and innate immunity in cancer.

Main Methods:

  • Literature review of recent studies on replication stress.
  • Analysis of endogenous replication impediments and their effects.
  • Examination of the interplay between stalled forks and innate immune responses.

Main Results:

  • Replication stress significantly increases genomic instability in cancer.
  • Endogenous impediments critically affect replication fork velocity.
  • Stalled forks can activate innate immunity, influencing the tumor microenvironment.

Conclusions:

  • Replication stress is a critical factor in cancer progression and genomic instability.
  • Targeting replication stress and its immune interactions presents novel therapeutic opportunities for cancer treatment.