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Published on: February 13, 2019
Functional and physical interaction between Rad24 and Rfc5 in the yeast checkpoint pathways
T Shimomura1, S Ando, K Matsumoto
1Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-0814, Japan.
Molecular and Cellular Biology
|August 26, 1998
Summary
RAD24 gene dosage suppresses replication factor C (RFC) complex defects in yeast DNA repair and replication checkpoints. This study reveals a physical and functional interaction between Rad24 and Rfc5 in DNA damage response pathways.
Area of Science:
- Molecular Biology
- Cellular Biology
- Genetics
Background:
- The replication factor C (RFC) complex, specifically its RFC5 subunit, is crucial for DNA replication checkpoints responding to damage.
- RAD24 is known to be involved in DNA damage checkpoint control.
Purpose of the Study:
- To investigate the relationship between RFC5 and RAD24 in yeast DNA repair and checkpoint pathways.
- To characterize the functional and physical interactions between Rad24 and Rfc5.
Main Methods:
- Genetic analysis of yeast mutants (rfc5-1) and gene overexpression (RAD24).
- Assays for DNA-damaging agent sensitivity and Rad53 phosphorylation.
- Co-sedimentation and interaction studies of Rad24 and RFC subunits.
Main Results:
- RAD24 overexpression suppressed the sensitivity of rfc5-1 mutants to DNA-damaging agents.
- RAD24 overexpression restored DNA damage-induced Rad53 phosphorylation in rfc5-1 mutants.
- Rad24 physically interacts with RFC subunits Rfc2 and Rfc5 and is required for Rad53 regulation.
Conclusions:
- Rad24 and Rfc5 exhibit both physical and functional interactions within DNA checkpoint pathways.
- RAD24 plays a significant role in regulating Rad53 phosphorylation in response to DNA damage.
- The interaction between Rad24 and Rfc5 is essential for both replication block and DNA damage checkpoints.
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