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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
Replication in Eukaryotes01:29

Replication in Eukaryotes

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
Eukaryotic replication follows many of the same...
Replication in Eukaryotes02:31

Replication in Eukaryotes

Overview
Replication in Eukaryotes02:31

Replication in Eukaryotes

Overview
Replication in Eukaryotes01:29

Replication in Eukaryotes

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
Eukaryotic replication follows many of the same...
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.

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Related Experiment Video

Updated: Jul 1, 2026

Imaging Replicative Domains in Ultrastructurally Preserved Chromatin by Electron Tomography
14:56

Imaging Replicative Domains in Ultrastructurally Preserved Chromatin by Electron Tomography

Published on: May 20, 2022

Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.

Kate Liddiard1, Emmon Coral2, Harsh Bhatt2

  • 1Cardiff University School of Medicine liddiardk@cardiff.ac.uk.

Genome Research
|June 29, 2026
PubMed
Summary
This summary is machine-generated.

Replicative crisis, driven by telomere shortening, dramatically alters cancer genome structure. This study reveals how chromatin changes and extrachromosomal DNA shifts during crisis offer new biomarkers for cancer progression.

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Single-Molecule Real-Time Visualization of DNA Unwinding by CMG Helicase
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Single-Molecule Real-Time Visualization of DNA Unwinding by CMG Helicase

Published on: September 27, 2024

Related Experiment Videos

Last Updated: Jul 1, 2026

Imaging Replicative Domains in Ultrastructurally Preserved Chromatin by Electron Tomography
14:56

Imaging Replicative Domains in Ultrastructurally Preserved Chromatin by Electron Tomography

Published on: May 20, 2022

Single-Molecule Real-Time Visualization of DNA Unwinding by CMG Helicase
07:37

Single-Molecule Real-Time Visualization of DNA Unwinding by CMG Helicase

Published on: September 27, 2024

Area of Science:

  • Genomics
  • Cancer Biology
  • Molecular Biology

Background:

  • Telomere dysfunction is a hallmark of cancer, driving genomic instability.
  • The precise mechanisms and consequences of telomere-driven replicative crisis on genome architecture are not fully understood.
  • Novel biomarkers for cellular stress in cancer progression remain to be discovered.

Purpose of the Study:

  • To investigate the genomic and architectural changes during telomere-driven replicative crisis.
  • To identify potential biomarkers associated with cellular stress and cancer progression.

Main Methods:

  • High-resolution multi-omics analyses in a human fibroblast model of crisis.
  • Development of a novel chromatin conformation capture procedure to study telomere interactions.
  • Targeted capture panel and short/long-read sequencing for repetitive and extrachromosomal DNA analysis.

Main Results:

  • Identified large-scale structural genomic changes and a shift from local to distant genomic interactions during crisis.
  • Revealed crisis-induced chromatin decompaction, altered gene expression, and ageing signatures in centromeric sequences.
  • Observed significant transitions in extrachromosomal circular DNA (eccDNA) abundance, complexity, and sequence content during crisis.

Conclusions:

  • Telomere dysfunction and transcription-driven chromatin reorganization link replication stress to genome instability.
  • These processes facilitate telomere fusions, eccDNA emergence, and overall genomic instability.
  • The identified changes represent dynamic biomarkers of cellular stress relevant to cancer progression.