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Related Concept Videos

The DNA Replication Fork01:02

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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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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).
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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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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 Replicating Timing Combined with Fluorescent In situ Hybridization
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Low Replicative Stress Triggers Cell-Type Specific Inheritable Advanced Replication Timing.

Lilas Courtot1, Elodie Bournique1, Chrystelle Maric2

  • 1Centre de Recherches en Cancérologie de Toulouse (CRCT), UMR1037 Inserm, University Paul Sabatier III, ERL5294 CNRS, 2 Avenue Hubert Curien, 31037 Toulouse, France.

International Journal of Molecular Sciences
|June 2, 2021
PubMed
Summary
This summary is machine-generated.

Low replication stress can advance DNA replication timing, particularly in heterochromatin. These replication timing advances can be inherited, impacting cellular identity and gene expression in daughter cells.

Keywords:
DNA damageDNA replication stressDNA replication timingchromatin accessibility

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Area of Science:

  • Cellular Biology
  • Genetics
  • Epigenetics

Background:

  • DNA replication timing (RT) is a cell-type-specific process.
  • Low replication stress typically causes RT delays, but can also cause uncharacterized RT advances.
  • Replication stress impacts genetic instability and cellular identity.

Purpose of the Study:

  • To characterize RT advances induced by low replication stress.
  • To investigate the cell-type specificity and genomic regions involved in RT advances.
  • To determine if RT advances can be inherited by subsequent cell generations.

Main Methods:

  • Whole genome RT was monitored in six human cell lines.
  • Cells were treated with low doses of aphidicolin to induce replication stress.
  • Inheritance of RT advances and associated molecular changes were analyzed.

Main Results:

  • RT advances were observed and found to be cell-type-specific, involving large heterochromatin domains.
  • Major late to early RT advances were inherited by the next cellular generation.
  • Inherited RT advances correlated with increased chromatin accessibility, altered origin landscape, and modified gene expression.

Conclusions:

  • Low replication stress can induce heritable RT advances, impacting cellular identity.
  • RT advances in heterochromatin represent a novel mechanism by which cells adapt to stress.
  • This study reveals a new layer of epigenetic regulation influencing cellular inheritance and gene expression patterns.