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Updated: Jun 22, 2026
12:02
Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
DNA damage checkpoints inhibit mitotic exit by two different mechanisms.
Fengshan Liang1, Yanchang Wang
1Department of Biomedical Sciences, College of Medicine, Florida State University, 1115 West Call Street, Tallahassee, FL 32306, USA.
Molecular and Cellular Biology
|May 9, 2007
Summary
DNA damage triggers distinct pathways in yeast to halt cell cycle progression. The Rad53 pathway inhibits the mitotic exit network (MEN), while Chk1 prevents early release of Cdc14 phosphatase.
Area of Science:
- Cell biology
- Molecular biology
- Genetics
Background:
- Cyclin-dependent kinases (CDKs) regulate cell cycle progression.
- Mitotic exit pathways in Saccharomyces cerevisiae, FEAR and MEN, inactivate CDKs.
- DNA damage checkpoints (Chk1, Rad53) prevent cell cycle progression.
Purpose of the Study:
- Investigate how yeast cells negatively regulate mitotic exit upon DNA damage.
- Elucidate the roles of Chk1 and Rad53 pathways in controlling mitotic exit.
Main Methods:
- Yeast genetics
- Cell cycle analysis
- Checkpoint activation studies
Main Results:
- Rad53 inhibits the MEN pathway, preventing mitotic exit.
- Chk1 prevents FEAR pathway-mediated Cdc14 release during DNA damage.
- Rad53 regulates MEN independently of Cdc5, alleviating Bfa1 inhibition.
Conclusions:
- Yeast employs two distinct pathways (Rad53-MEN and Chk1-FEAR) to suppress mitotic exit during DNA damage.
- These findings reveal novel regulatory mechanisms of cell cycle control in response to genotoxic stress.
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