RESUMO
BACKGROUND: Powdery mildew caused by Blumeria graminis f. sp. hordei (Bgh) is a constant threat to barley production but is generally well controlled through combinations of host genetics and fungicides. An epidemic of barley powdery mildew was observed from 2007 to 2013 in the West Australian grain belt. RESULTS: We collected isolates across Australia, examined their sensitivity to demethylation inhibitor (DMI) fungicides and sequenced the Cyp51B target gene. Five amino acid substitutions were found, of which four were novel. The most resistant haplotypes increased in prevalence from 0% in 2009 to 16% in 2010 and 90% in 2011. Yeast strains expressing the Bgh Cyp51 haplotypes replicated the altered sensitivity to various DMIs and these results were complemented by in silico protein docking studies. CONCLUSIONS: The planting of very susceptible cultivars and the use of a single fungicide mode of action was followed by the emergence of a major epidemic of barley powdery mildew. Widespread use of DMI fungicides led to the selection of Bgh isolates carrying both the Y137F and S524T mutations, which, as in Zymoseptoria tritici, account for resistance factors varying from 3.4 for propiconazole to 18 for tebuconazole, the major azoles used at that time in WA. © 2019 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
