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J. Biol. Chem., Vol. 278, Issue 32, 29760-29768, August 8, 2003

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Gts1p Activates SNF1-dependent Derepression of HSP104 and TPS1 in the Stationary Phase of Yeast Growth^*

So-ichi Yaguchi and Kunio Tsurugi 

From the Department of Biochemistry 2, University of Yamanashi, Faculty of Medicine, 1110 Shimokato, Tamaho, Yamanashi 409-3898, Japan

We previously reported that the GTS1 product, Gts1p, plays an important role in the regulation of heat tolerance of yeast under glucose-limited conditions in either batch or continuous culture. Here we show that heat tolerance was decreased in GTS1-deleted and increased in GTS1-overexpressing cells under glucose-derepressed conditions during the batch culture and that the disruption of SNF1, a transcriptional activator of glucose-repressible genes, diminished this effect of GTS1. Intracellular levels of Hsp104 and trehalose, which were reportedly required for the acquisition of heat tolerance in the stationary phase of cell growth, were affected in both GTS1 mutants roughly in proportion to the gene dosage of GTS1, whereas those of other Hsps were less affected. The mRNA levels of genes for Hsp104 and trehalose-6-phosphate synthase 1 changed as a function of GTS1 gene dosage. The Q-rich domain of Gts1p fused with the DNA-binding domain of LexA activated the transcription of the reporter gene LacZ, and Gts1p lacking the Q-rich domain lost the activation activity of HSP104 and TPS1. Furthermore, Gts1p bound to subunits of Snf1 kinase, whereas it did not bind to DNA. Therefore, we suggested that GTS1 increases heat tolerance by mainly activating Snf1 kinase-dependent derepression of HSP104 and TPS1 in the stationary phase of yeast growth.

Received for publication, February 10, 2003 , and in revised form, May 22, 2003.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel./Fax: 81-55-273-6784; E-mail: ktsurugi{at}res.yamanashi-med.ac.jp.

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