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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

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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

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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.
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Translesion DNA Polymerases02:10

Translesion DNA Polymerases

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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Updated: Sep 18, 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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DNA Damage and Replication Stress Checkpoints.

Luke A Yates1,2,3, Xiaodong Zhang1,2, Peter M Burgers4

  • 1DNA Processing Machines Laboratory, Francis Crick Institute, London, United Kingdom.

Annual Review of Biochemistry
|June 20, 2025
PubMed
Summary
This summary is machine-generated.

DNA damage checkpoints prevent genomic instability and cancer by pausing cell division for DNA repair. This review details the molecular mechanisms of these crucial checkpoints, focusing on ATM and ATR kinases.

Keywords:
ATMTel1 kinaseATRMec1 kinaseDNA metabolismcell cycle checkpointsreplication stresssignaling cascades

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA damage checkpoints are essential for maintaining genomic stability.
  • Defects in these checkpoints are linked to cancer development.
  • Understanding checkpoint mechanisms is vital for cancer precision medicine.

Purpose of the Study:

  • To review the current mechanistic understanding of eukaryotic DNA damage checkpoints.
  • To highlight the roles of ATM (Tel1) and ATR (Mec1) sensor kinases.
  • To emphasize structure-function and cellular studies of checkpoint components.

Main Methods:

  • Review of cutting-edge structural techniques.
  • Analysis of molecular insights into checkpoint signaling.
  • Integration of structure-function and cellular studies.

Main Results:

  • Detailed mechanistic understanding of DNA damage checkpoint signaling.
  • Elucidation of the roles of ATM and ATR kinases in response to DNA damage and replication stress.
  • Insights into the coordinated signaling pathways.

Conclusions:

  • DNA damage checkpoints are critical regulators of cell cycle progression.
  • ATM and ATR kinases are key sensors in these pathways.
  • Structural and cellular studies provide a deeper understanding of checkpoint function and its relevance to cancer.