M. Asadollahi - Department of Biochemical Engineering, Faculty of Science and Technology, University of Debrecen, ‎Egyetem tér ۱., ۴۰۳۲ Debrecen, Hungary.‎
A. Szojka - Department of Biochemical Engineering, Faculty of Science and Technology, University of Debrecen, ‎Egyetem tér ۱., ۴۰۳۲ Debrecen, Hungary.‎
E. Fekete - Department of Biochemical Engineering, Faculty of Science and Technology, University of Debrecen, ‎Egyetem tér ۱., ۴۰۳۲ Debrecen, Hungary.‎
L. Karaffa - Department of Biochemical Engineering, Faculty of Science and Technology, University of Debrecen, ‎Egyetem tér ۱., ۴۰۳۲ Debrecen, Hungary.‎
F. Takács - Research and Extension Centre for Fruit Growing, Vadastag ۲, H-۴۲۴۴ Újfehértó, Hungary.‎
M. Flipphi - Department of Biochemical Engineering, Faculty of Science and Technology, University of Debrecen, ‎Egyetem tér ۱., ۴۰۳۲ Debrecen, Hungary.‎
E. Sándor - Institute of Food Processing, Quality Assurance and Microbiology, Faculty of Agricultural and Food ‎Sciences and Environmental Management, University of Debrecen, Böszörményi út ۱۳۸., ۴۰۳۲ Debrecen, ‎Hungary.‎

Quinol oxidation inhibitors (QoIs) are one of the most important classes of fungicides used in agriculture. They block electron transfer between cytochrome b and cytochrome c۱, thereby impeding the production of ATP via oxidative phosphorylation. QoI fungicides are generally at high risk of provoking resistance in fungal phytopathogens. Resistance has been reported in more than thirty species, amongst others, in Botrytis cinerea. In various QoI-resistant monosporic B. cinerea isolates from Hungary, a G-to-C point mutation was identified in the mitochondrial gene that encodes the QoI target, cytochrome b, resulting in a glycine to alanine substitution at position ۱۴۳ (G۱۴۳A). Analysis of Hungarian group I and group II strains further indicated the frequent occurrence of an additional group I-type intron in the cytb gene directly downstream of the glycine-۱۴۳ codon. Mutual presence of distinct mitochondrial DNAs specifying different cytb alleles (heteroplasmy) has also been detected in monosporic strains. Remarkably, a number of group II field isolates were found to be highly resistant to azoxystrobin although they did not appear to carry the G-to-C mutation (G۱۴۳A) generally associated with fungal QoI-resistance.

Azoxystrobin resistance, Botrytis pseudocinerea, Group I intron, Heteroplasmy, Quinol ‎Oxidation Inhibitor.‎