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Published on: October 21, 2022
The yeast CDC16 and CDC27 genes restrict DNA replication to once per cell cycle
1Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA.
Cell
|April 5, 1996
Summary
New genes CDC16 and CDC27 in yeast limit DNA replication. Mutants overreplicate DNA up to 8C within one cell cycle, highlighting their role in cell cycle control.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- DNA replication must be tightly regulated to occur only once per cell cycle.
- The cell cycle control system ensures genomic stability by preventing DNA overreplication.
- Understanding the genes involved in replication control is crucial for cell cycle research.
Purpose of the Study:
- To identify genes in Saccharomyces cerevisiae that regulate DNA replication.
- To investigate the mechanisms by which DNA overreplication occurs.
- To characterize new conditional alleles affecting DNA replication.
Main Methods:
- Genetic screening for DNA overreplication mutants in S. cerevisiae.
- Analysis of DNA content (e.g., 8C DNA accumulation).
- Cell cycle analysis, including monitoring mitosis and START.
- Investigating checkpoint activation (e.g., MEC1 checkpoint).
- Assessing cyclin-dependent kinase activity (e.g., Clb2-Cdc28).
Main Results:
- CDC16 and CDC27 were identified as essential genes for limiting DNA replication to once per cell cycle.
- A screen identified new conditional alleles causing DNA overreplication (up to 8C).
- Overreplication occurred within a single cell cycle, involving all chromosomes, and could trigger the MEC1 checkpoint.
- Elevated Clb2-Cdc28 activity persisted in overreplicating cells.
- These findings differentiate CDC16/CDC27 roles from mutants causing overreplication via aberrant mitosis.
Conclusions:
- CDC16 and CDC27 play a critical role in preventing DNA overreplication in S. cerevisiae.
- These genes may function by regulating the targeted proteolysis of S phase initiators.
- The study provides new insights into the molecular mechanisms of cell cycle control and DNA replication fidelity.
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