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Related Concept Videos

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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S-Cdk Initiates DNA Replication02:38

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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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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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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.
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Chromosome Replication02:31

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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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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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Updated: Oct 17, 2025

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Preventing excess replication origin activation to ensure genome stability.

Bhushan L Thakur1, Anagh Ray1, Christophe E Redon1

  • 1Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Trends in Genetics : TIG
|October 9, 2021
PubMed
Summary

Cells tightly control DNA replication to prevent errors. When these controls fail in cancer, excess DNA synthesis and genomic instability arise, offering potential therapeutic targets.

Keywords:
DNA damagedormant originsextrachromosomal DNAextrachromosomal circular DNAgenomic instabilityoverreplicationre-replicationreplication origins

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Biology

Background:

  • Cells possess regulatory pathways to ensure accurate DNA replication and prevent excessive DNA synthesis.
  • Protein-DNA interactions and pre-replication complex modifications are key mechanisms controlling DNA replication initiation.
  • Dysregulation of these controls in cancer leads to replication stress and genomic instability.

Purpose of the Study:

  • To review the molecular pathways governing replication origin dormancy and activation.
  • To explore how cancer cells exploit excess DNA synthesis and recombination.
  • To identify therapeutic strategies targeting genomic instability in cancer.

Main Methods:

  • Review of molecular pathways modulating replication origin dormancy.
  • Analysis of mechanisms preventing excess origin activation.
  • Examination of processes for detecting, encapsulating, and eliminating excess DNA.

Main Results:

  • Excess DNA synthesis is inhibited by specific protein-DNA interactions and pre-replication complex modifications.
  • Cancer cells often exhibit uncontrolled replication origin activation, leading to extrachromosomal DNA amplification.
  • Recombination-mediated processes can amplify extrachromosomal DNA, generating chromosomal translocations.
  • Genomic instability resulting from excess replication origin activation presents a therapeutic vulnerability.

Conclusions:

  • Understanding replication control mechanisms is crucial for comprehending cancer development.
  • Targeting pathways that prevent excess DNA replication and manage genomic instability holds therapeutic promise for cancer treatment.