SummaryIn an effort to understand how an accurate level of stress-specific expression is obtained, we studied the promoter of the yeast HSP104 gene. Through 5¢ deletions, we defined a 334 bp fragment upstream of the first coding AUG as sufficient and essential for maximal basal activity and a 260 bp fragment as sufficient and essential for heat shock responsiveness. These sequences contain heat shock elements (HSEs) and stress response elements (STREs) that cooperate to achieve maximal inducible expression. However, in the absence of one set of factors (e.g. in msn2Dmsn4D cells) proper induction is obtained exclusively through HSEs. We also show that HSP104 is constitutively derepressed in ras2D cells. This derepression is achieved exclusively through activation of STREs, with no role for HSEs. Strikingly, in ras2Dmsn2Dmsn4D cells the HSP104 promoter is also derepressed, but in this strain derepression is mediated through HSEs, showing the flexibility and adaptation of the promoter. Thus, appropriate transcription of HSP104 is usually obtained through cooperation between the Msn2/4/STRE and the HSF/ HSE systems, but each factor could activate the promoter alone, backing up the other. Transcription control of HSP104 is adaptive and robust, ensuring proper expression under extreme conditions and in various mutants. IntroductionIn order to survive under suboptimal conditions, cells have developed several types of responses, known as the cellular stress responses. A major stress response is the induction of expression (to a high level) of protective and repair systems, capable of combating the particular stress or damage. Another simultaneous response is the induc- of stresses ranging from oxidative and osmolar stress, to nitrogen starvation (Boy-Marcotte et al., 1998;Moskvina et al., 1998;Treger et al., 1998a). In addition, HSEs are found in the promoters of a limited number of stress genes (mainly encoding Hsps) whereas STREs are more abundant (Moskvina et al., 1998;Treger et al., 1998a). The STRE system could therefore be considered a general, non-specific stress response (Ruis and Schuller, 1995;Siderius and Mager, 1997).STREs serve as a binding site for transcriptional activators, containing Cys 2 His 2 zinc fingers. Two such factors, known as Msn2p and Msn4p, are activators of many STRE-containing genes (Martinez-Pastor et al., 1996;Schmitt and McEntee, 1996). Hot1p and Msn1p also activate some STRE-driven genes (Rep et al., 2000). A msn2Dmsn4D double mutant shows up to 10-fold reductions in the basal and induced expression of many stressrelated genes (Boy-Marcotte et al., 1996;Martinez-Pastor et al., 1996;Moskvina et al., 1998;Gasch et al., 2000;Causton et al., 2001). Notably, in spite of the central role of Msn2/4p in the stress response, expression of many stress genes is not totally abolished in msn2Dmsn4D cells (Treger et al., 1998b;Boy-Marcotte et al., 1999;Simon et al., 1999;Gasch et al., 2000;Rep et al., 2000). Furthermore, activation of genes such as HSP104, UBI4 and HSP78 is similar in wild-type and ...
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