Mechanisms influencing the sensitivity of Alternaria solani causing early blight on potato towards demethylation inhibitors

Abstract

Early blight, caused by A. solani, is one of the major pathogens in potato. Besides agronomical measures, it is controlled by foliar fungicides. QoIs, SDHIs and DMIs represent three major fungicide groups, and the most important resistance mechanism is the target site mutation. DMIs inhibit the sterol 14α-demethylase (CYP51), a key enzyme in the fungal sterol biosynthesis pathway. To date, no resistance mechanisms have been detected. The aim of this work was to determine target site mutations in CYP51 gene conferring DMI adaptation. Mutations L143F+G446S and G462S have been identified being responsible for reduced sensitivity to DMIs. A CYP51 gene transfer were performed and showed increased EC50 values for mutation L143F and G446S for difenoconazole and mefentrifluconazole. In vivo fitness tests were conducted and led to the assumption that haplotype L143F+G446S is linked to significant fitness penalties.