Cytochrome b gene structure and consequences for resistance to Qo inhibitor fungicides in plant pathogens
Cytochrome b gene structure and consequences for resistance to Qo inhibitor fungicides in plant pathogens
- Pest Management Science, 62(2), p.465-472, 2006 .
The cytochrome b (cyt b)gene structure was characterized for different agronomically important plant pathogens, such as Puccinia recondita f sp tritici (Erikss)CO Johnston, P graminis f sp tritici Erikss and Hennings, P striiformis f sp tritici Erikss, P coronata f sp avenae P Syd & Syd, P hordei GH Otth, P recondita f sp secalis Roberge, P sorghi Schwein, P horiana Henn, Uromyces appendiculatus (Pers)Unger, Phakopsora pachyrhizi Syd P & Syd, Hemileia vastatrix Berk & Broome, Alternaria solani Sorauer, A alternata (Fr)Keissl and Plasmopara viticola (Berk & Curt)Berlese de Toni. The sequenced fragment included the two hot spot regions in which mutations conferring resistance to QoI fungicides may occur. The cyt b gene structure of these pathogens was compared with that of other species from public databases, including the strobilurin-producing fungus Mycena galopoda (Pers)P Kumm, Saccharomyces cerevisiae Meyer ex Hansen, Venturia inaequalis (Cooke)Winter and Mycosphaerella fijiensis Morelet. In all rust species, as well as in A solani, resistance to QoI fungicides caused by the mutation G143A has never been reported. A type I intron was observed directly after the codon for glycine at position 143 in these species. This intron was absent in pathogens such as A alternata, Blumeria graminis (DC)Speer, Pyricularia grisea Sacc, Mycosphaerella graminicola (Fuckel)J Schr¨ ot,Mfijiensis, V inaequalis and P viticola, in which resistance to QoI fungicides has occurred and the glycine is replaced by alanine at position 143 in the resistant genotype. The present authors predict that a nucleotide substitution in codon 143 would prevent splicing of the intron, leading to a deficient cytochrome b, which is lethal. As a consequence, the evolution of resistance to QoI fungicides based on G143A is not likely to evolve in pathogens carrying an intron directly after this codon.
The cytochrome b (cyt b)gene structure was characterized for different agronomically important plant pathogens, such as Puccinia recondita f sp tritici (Erikss)CO Johnston, P graminis f sp tritici Erikss and Hennings, P striiformis f sp tritici Erikss, P coronata f sp avenae P Syd & Syd, P hordei GH Otth, P recondita f sp secalis Roberge, P sorghi Schwein, P horiana Henn, Uromyces appendiculatus (Pers)Unger, Phakopsora pachyrhizi Syd P & Syd, Hemileia vastatrix Berk & Broome, Alternaria solani Sorauer, A alternata (Fr)Keissl and Plasmopara viticola (Berk & Curt)Berlese de Toni. The sequenced fragment included the two hot spot regions in which mutations conferring resistance to QoI fungicides may occur. The cyt b gene structure of these pathogens was compared with that of other species from public databases, including the strobilurin-producing fungus Mycena galopoda (Pers)P Kumm, Saccharomyces cerevisiae Meyer ex Hansen, Venturia inaequalis (Cooke)Winter and Mycosphaerella fijiensis Morelet. In all rust species, as well as in A solani, resistance to QoI fungicides caused by the mutation G143A has never been reported. A type I intron was observed directly after the codon for glycine at position 143 in these species. This intron was absent in pathogens such as A alternata, Blumeria graminis (DC)Speer, Pyricularia grisea Sacc, Mycosphaerella graminicola (Fuckel)J Schr¨ ot,Mfijiensis, V inaequalis and P viticola, in which resistance to QoI fungicides has occurred and the glycine is replaced by alanine at position 143 in the resistant genotype. The present authors predict that a nucleotide substitution in codon 143 would prevent splicing of the intron, leading to a deficient cytochrome b, which is lethal. As a consequence, the evolution of resistance to QoI fungicides based on G143A is not likely to evolve in pathogens carrying an intron directly after this codon.