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. 2017 Jun 16;83(13):e00672-17. doi: 10.1128/AEM.00672-17

FIG 3.

FIG 3

Increased expression of TPO2-lacZ and YRO2-lacZ reporter genes due to an hrr25(E52D) mutation requires Haa1. Wild-type (BY4741) and isogenic haa1Δ (ZLY4043), hrr25(E52D) (ZLY4467), and hrr25(E52D) haa1Δ double mutant (ZLY4637) strains carrying centromeric plasmids encoding a TPO2-lacZ or YRO2-lacZ reporter gene were grown in MM4 without (A) and with (B) 60 mM acetic acid to the mid-logarithmic phase. β-Galactosidase activity assays were conducted as described in Materials and Methods. (C and D) An hrr25(E52D) mutation leads to increased nuclear localization of Haa1 in cells without acetic acid treatment. haa1Δ and hrr25(E52D) haa1Δ mutant strains expressing a functional Haa1-GFP fusion from a centromeric plasmid were grown in MM4 without and with 60 mM acetic acid. GFP fluorescence and differential interference contrast (DIC) images were captured as described in Materials and Methods.