Table 5.

β-Galactosidase activity conferred byARE1-lacZ and ARE2-lacZ promoter fusions in response to lesions or pharmacological inhibition of the ergosterol biosynthetic pathway

Strain or conditionβ-Galactosidase activity (fold change relative to wild type)d
ARE1-lacZARE2-lacZ
Wild-type BWG 1-7aa1.6 ± 0.2 (1.0)186 ± 17 (1.0)
erg2 mutant6.0 ± 0.9 (3.8)184 ± 30 (1.0)
erg3 mutant6.5 ± 0.5 (4.1)246 ± 25 (1.3)
erg6 mutant5.2 ± 0.9 (3.3)199 ± 30 (1.1)
Fenpropimorph addedb3.7 ± 0.3 (2.3)339 ± 30 (1.8)
Wild-type JR 527c1.7 ± 0.3 (1.0)80 ± 11 (1.0)
hmg1 mutant4.2 ± 0.5 (2.5)156 ± 20 (2.0)
hmg2mutant1.5 ± 0.2 (0.9)103 ± 16 (1.3)
  • a The erg mutants were created in the BWG 1-7a background.

  • b Fenpropimorph was added to strain BWG 1-7a at 0.5 μM, the cells were grown to 50% and then inhibited by the addition of 25 μM fenpropimorph, and the cells grew for an additional 18 h.

  • c JR527 is the wild-type strain isogenic to thehmg1 and hmg2 mutations.

  • d β-Galactosidase activity is reported as nanomoles ofo-nitrophenyl-β-d-galactopyranoside hydrolyzed per minute per milligram of protein and is the average of two independent transformants assayed in duplicate over 3 days.