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Molecular and Cellular Biology, May 2000, p. 3459-3469, Vol. 20, No. 10
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Fission Yeast Eso1p Is Required for Establishing
Sister Chromatid Cohesion during S Phase
Koichi
Tanaka,1
Toshihiro
Yonekawa,1,
Yosuke
Kawasaki,2
Mihoko
Kai,1,
Kanji
Furuya,2
Masaomi
Iwasaki,1,
Hiroshi
Murakami,1,§
Mitsuhiro
Yanagida,2 and
Hiroto
Okayama1,*
Department of Biochemistry and Molecular
Biology, Graduate School of Medicine, The University of Tokyo,
Bunkyo-ku, Tokyo 113-0033,1 and
Department of Gene Mechanisms, Graduate School of
Biostudies, Kyoto University, Sakyo-ku, Kyoto
606-8502,2 Japan
Received 29 November 1999/Returned for modification 10 January
2000/Accepted 28 February 2000
Sister chromatid cohesion is essential for cell viability. We have
isolated a novel temperature-sensitive lethal mutant named eso1-H17 that displays spindle assembly
checkpoint-dependent mitotic delay and abnormal chromosome segregation.
At the permissive temperature, the eso1-H17 mutant shows
mild sensitivity to UV irradiation and DNA-damaging chemicals. At the
nonpermissive temperature, the mutant is arrested in M phase with a
viability loss due to a failure to establish sister chromatid cohesion
during S phase. The lethal M-phase arrest phenotype, however, is
suppressed by inactivation of a spindle checkpoint. The
eso1+ gene is not essential for the onset and
progression of DNA replication but has remarkable genetic interactions
with those genes regulating the G1-S transition and DNA
replication. The N-terminal two-thirds of Eso1p is highly homologous to
DNA polymerase
of budding yeast and humans, and the C-terminal
one-third is homologous to budding yeast Eco1p (also called Ctf7p),
which is required for the establishment of sister chromatid cohesion.
Deletion analysis and determination of the mutation site reveal that
the function of the Eco1p/Ctf7p-homologous domain is necessary and
sufficient for sister chromatid cohesion. On the other hand, deletion
of the DNA polymerase
domain in Eso1p increases sensitivity to UV
irradiation. These results indicate that Eso1p plays a dual role during
DNA replication. The C-terminal region acts to establish sister
chromatid cohesion, and the N-terminal region presumably catalyzes
translesion DNA synthesis when template DNA contains lesions that block
regular DNA replication.
*
Corresponding author. Mailing address: Department of
Biochemistry and Molecular Biology, The University of Tokyo,
Graduate School of Medicine, Bunkyo-ku, Tokyo 113-0033, Japan.
Phone: 81-3-5689-0876. Fax: 81-3-3815-1490. E-mail:
okayama{at}m.u-tokyo.ac.jp.

Present address: Biochemical Research Laboratory, Eiken Chemical
Co. Ltd., Tochigi,
Japan.

Present address: Department of Pathology, School of Medicine,
Stanford University, Stanford, CA 94305-5324.
§
Present address: Cell Cycle Laboratory, Imperial Cancer Research
Fund, London WC2A 3PX, United
Kingdom.
Molecular and Cellular Biology, May 2000, p. 3459-3469, Vol. 20, No. 10
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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