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Related Concept Videos

S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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 replication.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

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 replication.
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...

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Chromosome Replicating Timing Combined with Fluorescent In situ Hybridization
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Replication factory activation can be decoupled from the replication timing program by modulating Cdk levels.

Alexander M Thomson1, Peter J Gillespie, J Julian Blow

  • 1Wellcome Trust Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee, Dundee DD1 5EH, Scotland, UK.

The Journal of Cell Biology
|January 20, 2010
PubMed
Summary
This summary is machine-generated.

Cyclin-dependent kinase (Cdk) activity modulates DNA replication timing in metazoans. Altering Cdk levels affects replication rate and DNA synthesis, impacting replication factories and origin firing during S phase.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Replication timing in metazoans involves ordered firing of origins in distinct subchromosomal domains during S phase.
  • Understanding the regulation of this program is crucial for comprehending genome stability and cell cycle control.

Purpose of the Study:

  • To investigate the role of cyclin-dependent kinase (Cdk) activity in regulating the metazoan replication timing program using Xenopus laevis egg extracts.
  • To determine how Cdk activity influences DNA replication rate, origin firing, and replication factory dynamics.

Main Methods:

  • Utilized Xenopus laevis egg extracts to accelerate the replication timing program in mammalian nuclei.
  • Manipulated cyclin-dependent kinase (Cdk) activity and monitored effects on replication rate, DNA synthesis, and replication factory formation.
  • Assessed the impact of checkpoint kinases on replication timing.

Main Results:

  • Replicative stress slowed the timing program via checkpoint activation, but inhibiting checkpoint kinases did not accelerate it in unperturbed S phase.
  • Lowering Cdk activity decreased replication rate and timing program progression; increasing Cdk activity enhanced them.
  • Altered Cdk activity modulated DNA synthesis amounts across different stages of the timing program, correlating with changes in active replication factories.

Conclusions:

  • Cyclin-dependent kinase (Cdk) activity plays a critical role in differentially regulating replication initiation, factory activation, and progression through the S phase timing program.
  • These findings offer new insights into the organizational mechanisms of chromosomal DNA replication during S phase.