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Published on: June 6, 2017
A cyclin-polarity feedback network ensures healthy cell proliferation
Landry Peyran1, Charles Lefranc1, Steven P Gygi2
1Univ. Bordeaux, CNRS, Institut de Biochimie et Génétique Cellulaires, UMR 5095; 33077, Bordeaux, France.
Nature Communications
|June 19, 2026
Summary
G1-cyclin-Cdc28Cdk1 helps correct cell polarity defects by boosting Cdc42 activation. However, irreparable defects lead to multinucleate cells due to enforced cell cycle commitment.
Area of Science:
- Cell Biology
- Molecular Biology
- Genetics
Background:
- Cell proliferation relies on coordinated cell cycle progression and polarity.
- In budding yeast, G1-cyclin-Cdc28Cdk1 establishes polarity by activating Cdc42, creating a growth and division axis.
- The direct role of Cdc28Cdk1 in rectifying polarity errors was previously unknown.
Purpose of the Study:
- To investigate the adaptive response of G1-cyclin-Cdc28Cdk1 in correcting cell polarity defects.
- To understand the mechanisms by which Cdc28Cdk1 participates in error correction related to cell polarity.
Main Methods:
- Analysis of G1-cyclin expression and localization.
- Investigation of Cdc42 activation dynamics.
- Cell cycle progression monitoring in response to polarity perturbations.
Main Results:
- Identified an adaptive response where G1-cyclin-Cdc28Cdk1 augments kinase activity towards Cdc42-activating substrates.
- Observed temporal and spatial cell cycle reconfiguration, including extended G1 cyclin expression and nucleocytoplasmic rerouting.
- Demonstrated that irreparable polarity defects, under high G1-cyclin levels, enforce cell cycle commitment, leading to multinucleate cells.
Conclusions:
- G1-cyclins not only initiate G1 events but also monitor their execution through feedback mechanisms.
- Cdc28Cdk1 plays a direct role in rectifying cell polarity errors, coordinating polarity with cell cycle progression.
- The cell employs a strategy with a potential cost of generating multinucleate cells when polarity defects are irreparable.
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