Evolved resistance to fungicides is a major problem limiting our ability to control agricultural, medical and veterinary pathogens and is frequently associated with substitutions in the amino acid sequence of the target protein. The convention for describing amino acid substitutions is to cite the wild‐type amino acid, the codon number and the new amino acid, using the one‐letter amino acid code. It has frequently been observed that orthologous amino acid mutations have been selected in different species by fungicides from the same mode of action class, but the amino acids have different numbers. These differences in numbering arise from the different lengths of the proteins in each species. The purpose of the present paper is to propose a system for unifying the labelling of amino acids in fungicide target proteins. To do this we have produced alignments between fungicide target proteins of relevant species fitted to a well‐studied ‘archetype’ species. Orthologous amino acids in all species are then assigned numerical ‘labels’ based on the position of the amino acid in the archetype protein. © 2016 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

More than 40 years have now passed since the development of the resistance of plant pathogens to fungicide treatments emerged as a major threat to crop protection. This opening chapter describes the appearance of resistant pathogen populations during this time, indicates their impact on crop disease management and reviews progress in detecting resistance and preventing or delaying its onset and spread. The evolution and management of resistance in different classes of fungicides (benzimidazoles, 2-aminopyrimidines, phenylamides, sterol demethylation inhibitors, dicarboximides and quinone outside inhibitors) are described.

Nineteen isolates of Rhizoctonia solani collected from different rice varieties grown in various regions of Punjab were studied for their morphological and pathological characterization. Majority of the isolates were fast growing with raised and fluffy colonies and hyphal width of 9.6 lm while four exhibited moderate growth rate. Colony colour in all except two isolates was light yellowish brown. While sclerotial number per 5.0 mm culture disc of the test isolates ranged between 2.1 and 11.2 mm, their size varied between 1.31 and 2.08 mm. Sclerotial colour in all except two isolates was dark brown and most of these were found scattered in the colony. There was no relationship between morphologically similar isolates and their pathogenic behaviour. Majority of the isolates produced lesion length between 45.6 and 58.2 mm on detached rice leaves (cv. PR116). Molecular characterization of genetic diversity in the test isolates was studied by using 10 inter simple sequence repeats (ISSR) and eight random amplified polymorphic DNA (RAPD) markers. The size of amplified DNA bands ranged from 0.25-3.0 to 0.5-4.0 kb with ISSR and RAPD markers, respectively. Combined data set of 155 DNA markers were analysed with UPGMA resulting five clusters with 49-89% genetic similarity. Most of the isolates showed grouping specific to the host variety. Out of these two types of DNA markers, RAPD markers were able to detect more genetic variability when compared to ISSR markers.

This chapter deals with the biochemical mode of action of quinone outside inhibitor (QoI) fungicides, which are respiration inhibitors; their fungicidal activity comes from their ability to inhibit mitochondrial respiration by binding at the so-called Qo site (the outer quinol-oxidation site or ubiquinol site) of the cytochrome bc1 enzyme complex (complex III), located in the inner mitochondrial membrane of fungi and other eukaryotes. It discusses the resistance risk to the QoIs; history of resistance to these fungicides; mutations associated with QoI resistance; and the monitoring for resistance to QoI fungicides. It is hoped that the experience of the QoI fungicides will help learning for the future novel classes of fungicides that will be introduced.

Asian soyabean rust, caused by the biotrophic fungus Phakopsora pachyrhizi, is considered the most damaging foliar disease of soyabean (Glycine max). This chapter describes the fungicides for soyabean rust control and the risk of resistance. The Asian soyabean rust in Brazil, the sensitivity monitoring programmes for this pathogen, and the management of its fungicide resistance are discussed.