Field resistance to Qol fungicides in Podosphaera fusca is not supported by typical mutations in the mitochondrial cytochrome b gene

• Published in: Pest management science 2008-07, Vol.64 (7), p.694-702
• Main Authors: FERNANDEZ-ORTUNO, Dolores, TORES, Juan A, DE VICENTE, Antonio, PEREZ-GARCIA, Alejandro
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Control; Fundamental and applied biological sciences. Psychology; Fungal plant pathogens; Fungi; Mutation; Pesticides; Phytopathology. Animal pests. Plant and forest protection; Plant mitochondria; Plant populations; Polymorphism; Resistance to control
• ISSN: 1526-498X; 1526-4998

A single nucleotide polymorphism in the mitochondrial cytochrome b gene confers resistance to strobilurin (Qol) fungicides in phytopathogenic fungi. Recent studies have revealed worrying levels of resistance to strobilurins in Podosphaera fusca (Fr.) U Braun & N Shishkoff comb. nov. [= Sphaerothecafusca (Fr.) S Blumer], the main causal agent of cucurbit powdery mildew in Spain. In the present study the underlying resistance mechanism to Qol fungicides in the Spanish populations of P. fusca was investigated. Analysis of the ... domains of cytochrome b in a collection of isolates revealed that none of the typical mutations conferring resistance to Qol, including the G143A and F129L substitutions, was present in the Qol-resistant isolates. Moreover, although different amino acid polymorphisms were observed in the two regions spanning the ... site, none of them consistently distinguished Qol-resistant from Qol-sensitive strains. Exposure to salicylhydroxamic acid (SHAM), a specific inhibitor of alternative oxidase, in the presence of trifloxystrobin did not have any effect on Qol resistance, ruling out alternative respiration as the mechanism of resistance. Sensitivity tests to a battery of respiration inhibitors revealed high levels of cross-resistance to all Qo-inhibitors tested but not to Qi-inhibitors, these features resembling those of a target-site-based resistance. The results indicate that the mechanism responsible for Qol resistance in P. fusca is not linked to typical mutations in cytochrome b gene and that the absence of the G143A substitution cannot be explained by an intron following codon 143. These are important observations, especially in relation to the possible molecular diagnosis of resistance. (ProQuest: ... denotes formulae/symbols omitted.)