FIG 6.

CgPDR1 or CgCDR1 disruption reverses azole resistance in the Cgfpr3Δ4Δ mutant. (A) Representative immunoblots showing H3K36me3 modification levels in the indicated C. glabrata strains. Log-phase cultures of wt and Cgfpr3Δ4Δ cells were either treated with 16 μg/ml fluconazole for 4 h or left untreated. Whole-cell lysates (50 μg protein) were resolved on 15% SDS-PAGE gels and probed with anti-H3K36me3, anti-H3, and anti-GAPDH antibodies. GAPDH serves as a loading control. The intensity signal in each lane was enumerated using ImageJ densitometry software, and the H3K36me3 methylation signal was normalized to the total H3 signal. Data (means ± SEM; n = 3 to 4) are plotted as a bar graph on the right side of the blot image and represent the percent changes in H3K36me3 levels in untreated Cgfpr3Δ4Δ and fluconazole-treated wt and Cgfpr3Δ4Δ cells, compared to untreated wt samples (considered 100%). (B) Serial dilution spot analysis to assess the fluconazole susceptibility of the indicated C. glabrata strains.