The genes being in the mitochondrial DNA primarily encode the enzymes of cellular respiration. Fungicides belonging to the family of quinol oxidase inhibitors (QoIs) play on important role in the protection against several plant diseases caused by fungi. These fungicides bind to the cytochrome bc1 complex so they block electron transport between cytochrome b and cytochrome c1. This way these fungicides inhibit the ATP synthesis consequently they inhibit the mitochondrial respiration. The QoI resistance has two mechanisms. One of them is the point mutation of the cytochrome b gene (CYTB), e.g. the substitution of a single glycine by alanine at position 143 results in high-resistance. The other is the cyanide-resistant alternative respiration sustained by the alternative oxidase.
In a cell there are several mitochondria. The phenomenon when the genomes of all mitochondria in the cell are identical is called homoplazmy. If in the cell there is wild and mutant mitochondrial DNA this is called heteroplasmy. Whether the mutation in the mitochondria causes fenotypical diversity or does not depend on the dose, i.e. it depends on the percentage of the changed mitochondrials. During our work we investigated Botrytis cinerea single spore isolates which have been collected in 2008-2009 on different host plants. Our goal was to decide whether heteroplasmy influences the level of resistance. We managed to detect the change of the level of heteroplasmy, so the change the level of the resistance due to the treatment with fungicide.