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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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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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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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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...
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Study of the DNA Damage Checkpoint using Xenopus Egg Extracts
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ATRX dysfunction induces replication defects in primary mouse cells.

David Clynes1, Clare Jelinska1, Barbara Xella1

  • 1MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford, United Kingdom.

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|March 22, 2014
PubMed
Summary
This summary is machine-generated.

The chromatin remodeler ATRX is crucial for DNA replication, particularly at repetitive DNA sequences. While ATRX deficiency causes DNA damage at telomeres, it does not activate the alternative lengthening of telomeres pathway in mouse cells.

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cell Biology

Background:

  • The ATRX protein is involved in alpha globin gene expression, progenitor cell proliferation, chromosome congression, and telomere maintenance.
  • ATRX mutations are found in tumors using telomerase-independent homologous recombination for telomere maintenance.
  • The precise mechanism linking ATRX dysfunction to diverse cellular phenomena remains unclear, but its role in replicating repetitive DNA is increasingly evident.

Purpose of the Study:

  • To investigate the direct role of ATRX in DNA replication using a mouse knockout model.
  • To determine if ATRX ablation is sufficient to trigger the alternative lengthening of telomeres (ALT) pathway.

Main Methods:

  • Generation and analysis of a mouse ATRX knockout model.
  • Assessment of DNA damage response at telomeres in mouse embryonic stem cells.
  • Evaluation of the activation of the alternative lengthening of telomeres pathway.

Main Results:

  • ATRX plays a direct role in facilitating DNA replication.
  • Ablation of ATRX leads to a DNA damage response specifically at telomeres.
  • Loss of ATRX alone is insufficient to activate the ALT pathway in mouse embryonic stem cells.

Conclusions:

  • ATRX is essential for efficient DNA replication, especially at repetitive DNA sequences.
  • While ATRX is involved in telomere maintenance and DNA damage response, its absence does not automatically induce the ALT pathway.
  • Further research is needed to elucidate the complete role of ATRX in genome stability and cancer biology.