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Molecular and Cellular Biology, September 2001, p. 5838-5845, Vol. 21, No. 17
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5838-5845.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Chl12 (Ctf18) Forms a Novel Replication Factor C-Related Complex
and Functions Redundantly with Rad24 in the DNA Replication
Checkpoint Pathway
Takahiro
Naiki,1
Tae
Kondo,1
Daisuke
Nakada,1
Kunihiro
Matsumoto,1,2 and
Katsunori
Sugimoto1,*
Division of Biological Science, Graduate
School of Science, Nagoya University,1 and
CREST, Japan Science and Technology Corporation
(JST),2 Chikusa-ku, Nagoya 464-0814, Japan
Received 5 March 2001/Returned for modification 23 April
2001/Accepted 4 June 2001
RAD24 has been identified as a gene essential for
the DNA damage checkpoint in budding yeast. Rad24 is structurally
related to subunits of the replication factor C (RFC) complex, and
forms an RFC-related complex with Rfc2, Rfc3, Rfc4, and Rfc5. The
rad24
mutation enhances the defect of
rfc5-1 in the DNA replication block
checkpoint, implicating RAD24 in this checkpoint.
CHL12 (also called CTF18) encodes
a protein that is structurally related to the Rad24 and RFC proteins.
We show here that although neither chl12
nor
rad24
single mutants are defective, chl12
rad24
double mutants become defective in the replication
block checkpoint. We also show that Chl12 interacts physically with
Rfc2, Rfc3, Rfc4, and Rfc5 and forms an RFC-related complex which is
distinct from the RFC and RAD24 complexes. Our results suggest that
Chl12 forms a novel RFC-related complex and functions redundantly with Rad24 in the DNA replication block checkpoint.
*
Corresponding author. Mailing address: Division of
Biological Science, Graduate School of Science, Nagoya University,
Chikusa-ku, Nagoya 464-0814, Japan. Phone: 81-52-789-2593. Fax:
81-52-789-2589. E-mail:
j46036a{at}nucc.cc.nagoya-u.ac.jp.
Molecular and Cellular Biology, September 2001, p. 5838-5845, Vol. 21, No. 17
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5838-5845.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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