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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.
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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.

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Hybrid Ensemble and Single-molecule Assay to Image the Motion of Fully Reconstituted CMG
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Cyclin A promotes S-phase entry via interaction with the replication licensing factor Mcm7.

Taku Chibazakura1, Kazuhiro Kamachi, Mayu Ohara

  • 1Department of Bioscience, Tokyo University of Agriculture, 1-1-1 Sakuragaoka, Setagaya-ku, Tokyo 156-8502, Japan. taku@nodai.ac.jp

Molecular and Cellular Biology
|November 17, 2010
PubMed
Summary

Cyclin A promotes cell cycle S-phase entry by interacting with Mcm7. A novel cyclin A mutant lacking this interaction impairs S-phase entry, highlighting Mcm7

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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cyclin A is crucial for initiating S-phase entry in mammalian cells.
  • The specific molecular targets of Cyclin A in this process remain largely undefined.

Purpose of the Study:

  • To identify critical targets of Cyclin A essential for S-phase entry.
  • To elucidate the role of Mcm7 in Cyclin A-mediated cell cycle progression.

Main Methods:

  • Generation of a novel human cyclin A mutant (CycA-C1) unable to promote S-phase entry.
  • Isolation and characterization of replication licensing factor Mcm7 and its interaction with wild-type and mutant Cyclin A.
  • Utilizing Mcm7 mutants (Mcm7-3) to rescue CycA-C1 function.
  • Employing RNA interference (RNAi) to assess endogenous Cyclin A function and Mcm7-3 rescue.

Main Results:

  • A novel human cyclin A mutant (CycA-C1) was created, which activates cyclin-dependent kinases but fails to induce S-phase entry.
  • Replication licensing factor Mcm7 was identified as an interaction partner of wild-type Cyclin A, but not the CycA-C1 mutant, within the chromatin fraction.
  • A specific Mcm7 mutant (Mcm7-3) capable of interacting with CycA-C1 was found to restore S-phase entry.
  • RNAi experiments confirmed that CycA-C1 is defective in endogenous Cyclin A function for S-phase entry, and this defect is suppressed by Mcm7-3.

Conclusions:

  • The interaction between Cyclin A and Mcm7 is essential for Cyclin A's function in promoting S-phase entry.
  • Mcm7 acts as a critical target or mediator for Cyclin A's role in initiating DNA replication.
  • This study defines a key molecular mechanism by which Cyclin A regulates cell cycle progression.