A cyclin-polarity feedback network ensures healthy cell proliferation
Abstract
Healthy proliferation requires the coordination of cell cycle progression with cell polarity. In budding yeast, polarity is established when G1-cyclin-Cdc28 Cdk1 triggers Cdc42 activation to generate a cell pole that is used as an axis for growth and division. While polarity defects delay the cell cycle temporally, permitting error correction, it is unknown if Cdc28 Cdk1 directly rectifies errant polarity. Here, we identify an adaptive response where G1-cyclin-Cdc28 Cdk1 participates in error correction via the augmentation of its kinase activity towards substrates that activate Cdc42. The response involves temporal and spatial cell cycle reconfiguration via extended G1 cyclin expression, nucleocytoplasmic rerouting and signaling. However, this strategy has a cost: if the defect is irreparable, high G1-cyclin levels enforce inexorable cell cycle commitment in the absence of a daughter cell, generating multinucleate cells. G1-cyclins therefore not only trigger G1 events, but also monitor their execution, employing feedback to coordinate polarity with cell cycle progression.
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BibTeX
@article{peyran2026cyclinpolarity,
title = {{A cyclin-polarity feedback network ensures healthy cell proliferation}},
author = {Landry Peyran and Charles Lefranc and Steven Gygi and Anne Royou and Derek Mccusker},
journal = {Nature Communications},
year = {2026},
month = oct,
doi = {10.1038/s41467-026-74596-7},
url = {https://hal.science/hal-05397698v2},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - A cyclin-polarity feedback network ensures healthy cell proliferation
AU - Landry Peyran
AU - Charles Lefranc
AU - Steven Gygi
AU - Anne Royou
AU - Derek Mccusker
PY - 2026
DA - 2026/10/12
JO - Nature Communications
DO - 10.1038/s41467-026-74596-7
UR - https://hal.science/hal-05397698v2
AB - Healthy proliferation requires the coordination of cell cycle progression with cell polarity. In budding yeast, polarity is established when G1-cyclin-Cdc28 Cdk1 triggers Cdc42 activation to generate a cell pole that is used as an axis for growth and division. While polarity defects delay the cell cycle temporally, permitting error correction, it is unknown if Cdc28 Cdk1 directly rectifies errant polarity. Here, we identify an adaptive response where G1-cyclin-Cdc28 Cdk1 participates in error correction via the augmentation of its kinase activity towards substrates that activate Cdc42. The response involves temporal and spatial cell cycle reconfiguration via extended G1 cyclin expression, nucleocytoplasmic rerouting and signaling. However, this strategy has a cost: if the defect is irreparable, high G1-cyclin levels enforce inexorable cell cycle commitment in the absence of a daughter cell, generating multinucleate cells. G1-cyclins therefore not only trigger G1 events, but also monitor their execution, employing feedback to coordinate polarity with cell cycle progression.
SN - 2041-1723
SN - 2041-1723
ER -