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M-Cdk Drives Transition Into Mitosis

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 Mitosis

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...

Inhibition of Cdk Activity

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 Activity

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...

Positive Regulator Molecules

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 Molecules

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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Related Experiment Video

Updated: Jun 23, 2026

Assessment of Sexual Behavior of Male Mice

Assessment of Sexual Behavior of Male Mice

Published on: March 5, 2020

Mice thrive without Cdk4 and Cdk2.

Cédric Barrière¹, David Santamaría, Antonio Cerqueira

¹Molecular Oncology, Centro Nacional de Investigaciones Oncológicas, E-28029 Madrid, Spain.

Molecular Oncology

|April 23, 2009

Summary

Cyclin-dependent kinases (Cdk) 4 and 2 are not essential for mammalian cell cycle progression or adult homeostasis. Mice lacking both Cdk4 and Cdk2 survive embryonic development but exhibit distinct phenotypes postnatally.

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Area of Science:

Cell Biology
Molecular Biology
Genetics

Background:

Mammalian cell division relies on sequential activation of Cyclin-dependent kinases (Cdks), primarily Cdk4, Cdk6, Cdk2, and Cdk1.
Viable mice lacking individual Cdk4, Cdk6, or Cdk2 suggest compensatory roles among these kinases.

Purpose of the Study:

To investigate the necessity of Cdk4 and Cdk2 in mammalian cell cycle regulation and organismal homeostasis.
To elucidate the functional redundancy or essentiality of Cdk4 and Cdk2 during embryonic development and adult life.

Main Methods:

Generation and analysis of mice with combined genetic deficiencies in Cdk4 and Cdk2.
Conditional ablation of Cdk2 in adult Cdk4-deficient mice.
Assessment of survival, physiological function, and cell cycle kinetics in mutant mice and embryonic fibroblasts.

Main Results:

Mice lacking both Cdk4 and Cdk2 (Cdk4(-/-);Cdk2(-/-)) survived embryonic development but died shortly after birth, suggesting a critical role during this period.
Conditional deletion of Cdk2 in adult Cdk4-deficient mice did not cause apparent abnormalities, and these mice recovered normally from partial hepatectomy.
Cdk4(-/-);Cdk2(-/-) embryonic fibroblasts exhibited immortalization, robust pRb phosphorylation, and normal S phase kinetics in culture.

Conclusions:

Cdk4 and Cdk2 are dispensable for the progression of the mammalian cell cycle in cultured cells and for maintaining adult homeostasis.
The combined absence of Cdk4 and Cdk2 leads to embryonic lethality, indicating essential roles during development that are compensated for in adult tissues.
These findings challenge the established view of Cdk4 and Cdk2 as universally essential drivers of the cell cycle in mammals.