Gene transcription changes dramatically in response to various stresses. This event is an obligatory step for adaptation of cells to certain environments. Endoplasmic reticulum (ER) oxidoreductin encoded by the ERO1 gene of the yeast Saccharomyces cerevisiae is essential for the formation of protein disulfide bonds in the ER and for cell viability. We show that transcription of ERO1 is regulated by two transcriptional activators in response to different stresses. In the unfolded protein response induced by the reductant dithiothreitol, transcription factor Hac1 activates ERO1 transcription through a sequence that diverges from the consensus Hac1-binding sequence. Heat shock transcription factor Hsf1 activates ERO1 in response to heat, ethanol, and oxidative stresses. Using cells containing mutations in the Hac1- and Hsf1-binding sequences of the chromosomal ERO1 promoter, we demonstrate that Hac1-regulated transcription of ERO1 confers resistance to dithiothreitol. Although mutations in the Hsf1-binding sequences do not affect the sensitivity of cells to heat, ethanol, or oxidative stresses, both the Hac1- and Hsf1-regulated pathways are critical for normal growth under complex stress conditions.

• PMID: 16292667
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Journal Article | Research Support, Non-U.S. Gov't

Authors

Takemori Y, Sakaguchi A, Matsuda S, Mizukami Y, Sakurai H

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