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Checkpoint controls in Schizosaccharomyces pombe: rad1.
R Rowley1, S Subramani, P G Young
1Department of Radiology, University of Utah Medical Center, Salt Lake City 84132.
The EMBO Journal
|April 1, 1992
Summary
The rad1-1 fission yeast mutant is defective in DNA damage and DNA synthesis checkpoint controls, leading to radiation sensitivity. This sensitivity is due to a failure to delay cell division, not impaired DNA repair.
Area of Science:
- Cell Biology
- Genetics
- Radiation Biology
Background:
- Cell cycle checkpoints ensure orderly progression through cell division.
- These checkpoints monitor DNA integrity and replication status.
- Failure of checkpoints can lead to genomic instability and cell death.
Purpose of the Study:
- To identify fission yeast mutants deficient in DNA damage-responsive checkpoint control.
- To characterize the rad1-1 mutant's response to DNA damage and replication stress.
- To investigate the role of rad1 in regulating cell cycle progression.
Main Methods:
- Screening of radiosensitive fission yeast mutants (rad series).
- Characterization of the rad1-1 mutant's cell cycle arrest response to irradiation and hydroxyurea.
- Assessment of rad1-1 radiosensitivity under non-dividing conditions.
Main Results:
- Five rad mutants deficient in DNA damage checkpoint control were identified.
- The rad1-1 mutant failed to arrest after irradiation and hydroxyurea treatment.
- rad1-1 radiosensitivity was reduced when DNA repair could occur in a non-dividing state, indicating repair proficiency.
- rad1 is required for G2-M progression, likely involving cdc2 activity.
Conclusions:
- The rad1 gene product is essential for both DNA damage and DNA synthesis checkpoint controls in fission yeast.
- The rad1-1 mutant exhibits radiosensitivity primarily due to checkpoint failure, not defective DNA repair.
- Checkpoint controls involving rad1 regulate G2-M progression, potentially through cdc2.