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Related Concept Videos

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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, a...
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 forks, one in...
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Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...
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Replication in Eukaryotes

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.
Many Proteins Orchestrate Replication at the Origin
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Replication in Eukaryotes02:31

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Overview
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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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Visualization of DNA Replication in the Vertebrate Model System DT40 using the DNA Fiber Technique
07:18

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Published on: October 27, 2011

DNA replication is intrinsically hindered in terminally differentiated myotubes.

Deborah Pajalunga1, Eleonora M R Puggioni, Alessia Mazzola

  • 1Department of Cell Biology and Neurosciences, National Institute of Health, Rome, Italy.

Plos One
|July 21, 2010
PubMed
Summary

Terminally differentiated cells cannot stably proliferate due to inherent state features, not reactivation methods. This explains why postmitotic cells fail to replicate DNA and proliferate, impacting tissue repair.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Terminally differentiated (TD) cells permanently exit the cell cycle.
  • TD cells cannot be induced to stably proliferate, often resulting in cell death or growth arrest.
  • The biological basis for this failure remains unexplained.

Purpose of the Study:

  • To investigate the reasons behind the inability of terminally differentiated cells to proliferate.
  • To identify the specific mechanisms preventing cell cycle reentry and sustained proliferation in TD cells.

Main Methods:

  • Depletion of p21 and p27 cell cycle inhibitors in TD mouse myotubes.
  • Reactivation of quiescent fibroblasts and myoblasts using similar methods.
  • Forced expression of E1A or cyclin D1 and cdk4 in TD and non-TD cells.

Main Results:

  • TD mouse myotubes, reactivated, failed to complete DNA replication, leading to DNA damage, apoptosis, or mitotic catastrophe.
  • Quiescent fibroblasts and myoblasts, reactivated similarly, successfully replicated DNA and proliferated.
  • Similar outcomes were observed when using E1A or cyclin D1/cdk4 for reactivation.

Conclusions:

  • The inability of TD cells to proliferate is due to intrinsic features of their differentiated state.
  • Proposed mechanisms suggest a general inability of TD cells across various types to proliferate.
  • This finding provides a basis for understanding postmitotic cell incompetence and its role in tissue repair.