Cdk1: unsung hero of S phase?

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Updated: Aug 29, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Marcin Pacek1, Tanya A Prokhorova, Johannes C Walter

  • 1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Cell Cycle (Georgetown, Tex.)
|January 31, 2004
PubMed

Insights

Cyclin-dependent kinase 2 (Cdk2) is not essential for cell proliferation. Mitotic kinases, Cdk1/Cyclin B and Cdk1/Cyclin A, can replace Cdk2

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Cyclin-dependent kinase 2 (Cdk2) has been traditionally considered essential for S phase progression and DNA replication.
  • Recent findings indicate that Cdk2 is dispensable for cell proliferation in mice.
  • This suggests the existence of alternative pathways that can regulate DNA replication.

Purpose of the Study:

  • To investigate the potential compensatory roles of other kinases in DNA replication.
  • To identify factors that can substitute for Cdk2 function in cell cycle regulation.
  • To explore the involvement of mitotic kinases in genome duplication.

Main Methods:

  • Experiments were conducted using Xenopus egg extracts.
  • The study focused on analyzing the activity of mitotic protein kinases.
  • Investigated the impact of Cdk1/Cyclin B and Cdk1/Cyclin A on DNA replication.

Main Results:

  • Mitotic protein kinases, specifically Cdk1/Cyclin B and Cdk1/Cyclin A, were identified as potential replacements for Cdk2.
  • These kinases were found to be capable of stimulating DNA replication in the absence of Cdk2.
  • The findings suggest an alternative mechanism for regulating DNA replication.

Conclusions:

  • Cdk1/Cyclin B and Cdk1/Cyclin A are likely candidates to compensate for Cdk2 function in DNA replication.
  • This discovery challenges the established role of Cdk2 as the sole regulator of S phase.
  • It is plausible that Cdk1 participates in genome duplication in wild-type cells, a role not previously recognized.

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