The likelihood of development of penconazole resistance in Venturia inaequalis was demonstrated using chemical mutagenesis of a
wild isolate of the pathogen not previously exposed to penconazole. Mutant strains displayed a high degree of resistance which was
stable. There was significant variation in the rate of total lipid and ergosterol biosyntheses between the resistant and sensitive
strains. Low uptake of penconazole due to energy-dependent efflux was found to be the mechanism underlying penconazole
resistance in the mutant strains, which also exhibited negatively correlated cross-resistance to mancozeb.