Fig. 7: Loss of viability induced by repression of erg6 is partially blocked by Hmg1 SSD mutation.

Models for sterol intermediate-induced negative feedback of Hmg1 through promotion of InsA binding under normal conditions (A), under triazole stress (B), and under doxycycline-mediated repression of erg6 expression in an erg6^pTetOff mutant (C). Illustration prepared using BioRender.com. D The parental control strains (hmg1^WT and hmg1^S305P) and their erg6^pTetOff derivatives (hmg1^WT/erg6^pTetOff and hmg1^S305P/erg6^pTetOff, respectively) were utilized for spot dilution assays on RPMI media (0.2% glucose, pH 7.0) with the indicated concentrations of doxycycline. Conidial inoculum concentrations for each strain were (from left to right) 5 × 10⁴, 5 × 103, 5 × 10², and 5 × 10¹ total conidia. Note the diminished ability of erg6 repression (i.e., increasing concentrations of exogenous doxycycline) to inhibit growth in the background of an hmg1 SSD mutant (hmg1^S305P).