Fig. 5: Mutations altering the transcriptional balance of insA-to-hmg1 disrupt normal response to triazole stress.
From: A secondary mechanism of action for triazole antifungals in Aspergillus fumigatus mediated by hmg1
A Schematic of promoter replacement mutations for hmg1 and insA using the hspA promoter (pHspA). Illustration prepared using BioRender.com. RT-qPCR analyses to confirm overexpression is shown for hmg1 (B) and insA (C). Expression levels from two independent mutants for each gene were compared to the parental control. Averaged data represent the mean ± standard deviation. n = three biologically independent samples and statistical analyses were performed by One-Way Anova followed by an unpaired T test with significance set at 0.05 and degrees of freedom equal to 10 for individual comparisons. Radial growth assays of the parental control, hmg1 overexpression (hmg1pHspA-1 and hmg1pHspA-2), and insA overexpression (insApHspA-1 and insApHspA-2) mutants to assess susceptibility changes are shown for rosuvastatin (D), terbinafine (E), and voriconazole (F). Conidia (5 ×103) from each strain were spot inoculated onto RPMI media (0.2% glucose, pH 7.0) containing the indicated amount of drug and plates were cultured for 72 hours at 37 °C. Source data are provided as a Source Data file.
