Molecular and Cellular Biology, September 1998, p. 5485-5491, Vol. 18, No. 9
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Division of Biological Science, Graduate School of Science, Nagoya University, Chikusa-ku, Nagoya 464-0814, Japan
Received 24 March 1998/Returned for modification 27 April 1998/Accepted 22 June 1998
The RFC5 gene encodes a small subunit of replication
factor C (RFC) complex in Saccharomyces cerevisiae and has
been shown to be required for the checkpoints which respond to
replication block and DNA damage. Here we describe the isolation of
RAD24, known to play a role in the DNA damage checkpoint,
as a dosage-dependent suppressor of rfc5-1. RAD24
overexpression suppresses the sensitivity of rfc5-1 cells
to DNA-damaging agents and the defect in DNA damage-induced Rad53
phosphorylation. Rad24, like Rfc5, is required for the regulation of
Rad53 phosphorylation in response to DNA damage. The Rad24 protein,
which is structurally related to the RFC subunits, interacts physically
with RFC subunits Rfc2 and Rfc5 and cosediments with Rfc5. Although the
rad24
mutation alone does not cause a defect in the
replication block checkpoint, it does enhance the defect in
rfc5-1 mutants. Furthermore, overexpression of
RAD24 suppresses the rfc5-1 defect in the
replication block checkpoint. Taken together, our results demonstrate a
physical and functional interaction between Rad24 and Rfc5 in the
checkpoint pathways.
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