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Journal of Bacteriology, September 2001, p. 4985-4993, Vol. 183, No. 17
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.17.4985-4993.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

The Saccharomyces cerevisiae Isw2p-Itc1p Complex Represses INO1 Expression and Maintains Cell Morphology

Minetaka Sugiyama and Jun-Ichi Nikawa*

Department of Biochemical Engineering and Science, Faculty of Computer Science and Systems Engineering, Kyushu Institute of Technology, Iizuka, Fukuoka 820-8502, Japan

Received 5 March 2001/Accepted 13 June 2001

In the yeast Saccharomyces cerevisiae, IRE1 encodes a bifunctional protein with transmembrane kinase and endoribonuclease activities. HAC1 encodes a transcription factor which has a basic leucine zipper domain. Both gene products play a crucial role in the unfolded protein response. Mutants in which one of these genes is defective also show the inositol-auxotrophic (Ino-) phenotype, but the reason for this has not been clear. To investigate the mechanism underlying the Ino- phenotype, we screened a multicopy suppressor gene which can suppress the Ino- phenotype of the Delta hac1 strain. We obtained a truncated form of the ITC1 gene that has a defect in its 3' region. Although the truncated form of ITC1 clearly suppressed the Ino- phenotype of the Delta hac1 strain, the full-length ITC1 had a moderate effect. The gene products of ITC1 and ISW2 are known to constitute a chromatin-remodeling complex (T. Tsukiyama, J. Palmer, C. C. Landel, J. Shiloach, and C. Wu, Genes Dev. 13:686-697, 1999). Surprisingly, the deletion of either ITC1 or ISW2 in the Delta hac1 strain circumvented the inositol requirement and caused derepression of INO1 even under repression conditions, i.e., in inositol-containing medium. These data indicate that the Isw2p-Itc1p complex usually represses INO1 expression and that overexpression of the truncated form of ITC1 functions in a dominant negative manner in INO1 repression. It is conceivable that the repressor function of this complex is regulated by the C-terminal region of Itc1p.

* Corresponding author. Mailing address: Department of Biochemical Engineering and Science, Faculty of Computer Science and Systems Engineering, Kyushu Institute of Technology, Iizuka, Fukuoka 820-8502, Japan. Phone: 81-948-29-7822. Fax: 81-948-29-7801. E-mail: nikawa{at}bse.kyutech.ac.jp.

Journal of Bacteriology, September 2001, p. 4985-4993, Vol. 183, No. 17
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.17.4985-4993.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.