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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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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
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of...
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Genome Copying Errors02:46

Genome Copying Errors

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DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
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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

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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DNA Damage Can Stall the Cell Cycle02:37

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Related Experiment Video

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Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization
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Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.

Aleix Bayona-Feliu1, Andrés Aguilera2,3

  • 1Department of Genetics, Microbiology and Statistics, Faculty of Biology, Universitat de Barcelona, Barcelona, Spain.

Bioessays : News and Reviews in Molecular, Cellular and Developmental Biology
|June 10, 2025
PubMed
Summary

Genome instability, driven by transcription-replication conflicts (TRCs), is linked to cancer. Understanding TRC processing and chromatin dynamics offers new anticancer strategies targeting these pathways.

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DNA damageR‐loopscancerchromatin remodelersgenome instabilityhistone modificationstranscription‐replication conflicts

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Genome instability (GIN) is a hallmark of cancer, promoting tumor evolution.
  • Transcription-replication conflicts (TRCs) are a major source of GIN, arising from conflicts between DNA replication and transcription.
  • Chromatin dynamics and epigenetic regulation are crucial for managing TRCs and maintaining genome integrity.

Purpose of the Study:

  • To review current knowledge on TRC processing and its role in genome integrity.
  • To explore the interplay between the DNA damage response (DDR), chromatin dynamics, and TRCs.
  • To discuss the clinical potential of targeting TRCs and epigenetic alterations in cancer therapy.

Main Methods:

  • Literature review of studies on transcription-replication conflicts.
  • Analysis of the role of chromatin dynamics in TRC resolution.
  • Examination of the link between epigenetic alterations and GIN in cancer.

Main Results:

  • TRCs are a significant source of DNA damage and GIN.
  • Defective TRC resolution compromises genome integrity.
  • Epigenetic deficiencies can lead to transcription-induced replication stress and DNA breaks.
  • Chromatin alterations correlate with increased mutation burden at TRC sites in tumors.

Conclusions:

  • TRCs are critical players in genome instability and cancer development.
  • Targeting TRCs and associated epigenetic signatures presents promising anticancer strategies.
  • Understanding the DDR and chromatin dynamics in TRC processing is key for therapeutic interventions.