FIG 1 .

The por1Δ mutation strongly affects lexAop-lacZ reporter activation by LexA-Snf1-G53R. (A) Strain CTY10-5d (WT) and its por1Δ and por2Δ mutant derivatives expressing LexA-Snf1-G53R were grown in selective SC medium containing high (2%) glucose to mid-log phase and then shifted for 3 h to an otherwise identical medium containing low (0.05%) glucose. β-Galactosidase activity was assayed in permeabilized cells and measured in Miller units (6 to 9 independent transformants per genotype). The graph shows the data under low-glucose conditions, and they are expressed as the percentage of the wild-type value. Under high-glucose conditions, all values were <3% of the wild-type value under low-glucose conditions. The mean wild-type value in low glucose was 278 Miller units. Error bars indicate standard errors. Statistical analyses were conducted using the two-tailed Student t test. Three pairwise tests were performed. The significance level for each test was Bonferroni adjusted from α = 0.05 to α_adj = 0.016. All three pairwise P values were less than α_adj (all P < 0.001). The plotted values are labeled with different lowercase letters (a, b, and c) to indicate that they are significantly different from each other. (B and C) Transformants were shifted to 0.05% glucose as described above and tested for Thr210 phosphorylation of the Snf1-G53R moiety (PT210) and total LexA-Snf1-G53R protein levels by immunoblotting. Vec, empty vector control.