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. 2015 Jun 15;26(12):2357–2374. doi: 10.1091/mbc.E14-12-1626

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© 2015 Bai et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 3: — The region between −654 and −626 in the STL1 promoter harbors an osmostress- and Hog1-responsive activity. The promoter is not induced via the Ras/Msn2/4 STRE system. (A) The indicated STL1 promoter fragments were subcloned upstream to the β-galactosidase gene (LacZ), and the resulting vectors were tested in wild-type (YPH102) cells exposed or not exposed to 0.7 M NaCl for 1 h. Left, promoter regions; right, the corresponding β-galactosidase activities. (B) Expression of intrinsically active Hog1, but not Hog1^WT, is sufficient to strongly induce the STL1 promoter. The –665STL1-LacZ construct was introduced into the indicated strains. Activity of β-galactosidase was assayed in cells after removal of methionine with or without addition of NaCl (both treatments were applied for 90 min). (C) STL1 promoter with a mutated STRE (the –704STL1^ctcgt-LacZ construct) is as responsive as the nonmutated promoter to NaCl (0.7 M, 60 min). (D) The –704STL1-LacZ construct is fully induced in cells of the indicated mutants but not in hog1∆ cells.