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Molecular and Cellular Biology, September 2000, p. 6399-6409, Vol. 20, No. 17
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Sgs1 Helicase Activity Is Required for Mitotic but Apparently Not for Meiotic Functions

Atsuko Miyajima,1 Masayuki Seki,2 Fumitoshi Onoda,2 Miwa Shiratori,2 Nao Odagiri,2 Kunihiro Ohta,3 Yoshiko Kikuchi,4 Yasuo Ohno,1 and Takemi Enomoto2,*

Division of Pharmacology, Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501,1 Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi 980-8578,2 Laboratory of Cellular and Molecular Biology, Institute of Physical and Chemical Research (RIKEN), Wako, Saitama 351-0198,3 Department of Biological Sciences, Graduate School of Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-0033,4 Japan

Received 20 April 2000/Returned for modification 23 May 2000/Accepted 7 June 2000

The SGS1 gene of Saccharomyces cerevisiae is a homologue for the Bloom's syndrome and Werner's syndrome genes. The disruption of the SGS1 gene resulted in very poor sporulation, and the majority of the cells were arrested at the mononucleated stage. The recombination frequency measured by a return-to-growth assay was reduced considerably in sgs1 disruptants. However, double-strand break formation, which is a key event in the initiation of meiotic DNA recombination, occurred; crossover and noncrossover products were observed in the disruptants, although the amounts of these products were slightly decreased compared with those in wild-type cells. The spores produced by sgs1 disruptants showed relatively high viability. The sgs1 spo13 double disruptants sporulated poorly, like the sgs1 disruptants, but spore viability was reduced much more than with either sgs1 or spo13 single disruptants. Disruption of the RED1 or RAD17 gene partially alleviated the poor-sporulation phenotype of sgs1 disruptants, indicating that portions of the population of sgs1 disruptants are blocked by the meiotic checkpoint. The poor sporulation of sgs1 disruptants was complemented with a mutated SGS1 gene encoding a protein lacking DNA helicase activity; however, the mutated gene could suppress neither the sensitivity of sgs1 disruptants to methyl methanesulfonate and hydroxyurea nor the mitotic hyperrecombination phenotype of sgs1 disruptants.

* Corresponding author. Mailing address: Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba Aramaki, Aoba-ku, Sendai, Miyagi 980-8578, Japan. Phone: (81)-22-217-6874. Fax: (81)-22-217-6873. E-mail: enomoto{at}mail.pharm.tohoku.ac.jp.

Molecular and Cellular Biology, September 2000, p. 6399-6409, Vol. 20, No. 17
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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