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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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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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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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Replication in Eukaryotes01:29

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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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Replication in Eukaryotes02:31

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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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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Related Experiment Video

Updated: Feb 17, 2026

Genome-wide Determination of Mammalian Replication Timing by DNA Content Measurement
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Genome-wide Determination of Mammalian Replication Timing by DNA Content Measurement

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DNA replication timing alterations identify common markers between distinct progeroid diseases.

Juan Carlos Rivera-Mulia1, Romain Desprat2, Claudia Trevilla-Garcia1

  • 1Department of Biological Science, Florida State University, Tallahassee, FL 32306.

Proceedings of the National Academy of Sciences of the United States of America
|December 3, 2017
PubMed
Summary

Progeroid syndromes share a distinct DNA replication timing (RT) signature, identifying the TP63 gene as an early biomarker. This discovery offers potential therapeutic targets for these rare aging disorders.

Keywords:
DNA replication timingRT signaturesTP63progeroid diseases

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Area of Science:

  • Genetics
  • Epigenetics
  • Molecular Biology

Background:

  • Progeroid syndromes are rare genetic disorders mimicking natural aging.
  • Existing research identified various causal mutations but lacked common molecular alterations.
  • DNA replication timing (RT) is a cell-specific epigenetic feature altered in disease.

Purpose of the Study:

  • To characterize DNA RT program alterations in Hutchinson-Gilford progeria syndrome (HGPS) and Rothmund-Thomson syndrome (RTS).
  • To compare these alterations with natural aging and cellular senescence.
  • To identify common molecular biomarkers for progeroid syndromes.

Main Methods:

  • Characterized DNA replication timing (RT) in cells from HGPS and RTS patients.
  • Compared RT profiles with healthy individuals, natural aging, and cellular senescence.
  • Utilized patient-derived induced pluripotent stem cells (iPSCs) to model disease onset and progression.

Main Results:

  • Identified a progeroid-specific RT signature common to HGPS and RTS patients.
  • The tumor protein p63 gene (TP63) was identified as a gene marker for progeroid syndromes.
  • Altered TP63 RT was an early event in disease progression, associated with altered TP63 isoform expression.

Conclusions:

  • DNA RT studies can identify novel biomarkers for rare diseases.
  • Abnormal TP63 RT is an early event in progeroid syndrome progression.
  • TP63 gene regulation presents a potential therapeutic target for progeroid syndromes.