Powdery mildew fungi (Erysiphales) are among the most common and important plant fungal pathogens. These fungi are obligate biotrophic parasites that attack nearly 10,000 species of angiosperms, including major crops, such as cereals and grapes. Although cultural and biological practices may reduce the risk of infection by powdery mildew, they do not provide sufficient protection. Therefore, in practice, chemical control, including the use of fungicides from multiple chemical groups, is the most effective tool for managing powdery mildew. Unfortunately, the risk of resistance development is high because typical spray programs include multiple applications per season. In addition, some of the most economically destructive species of powdery mildew fungi are considered to be high-risk pathogens and are able to develop resistance to several chemical classes within a few years. This situation has decreased the efficacy of the major fungicide classes, such as sterol demethylation inhibitors, quinone outside inhibitors and succinate dehydrogenase inhibitors, that are employed against powdery mildews. In this review, we present cases of reduction in sensitivity, development of resistance and failure of control by fungicides that have been or are being used to manage powdery mildew. In addition, the molecular mechanisms underlying resistance to fungicides are also outlined. Finally, a number of recommendations are provided to decrease the probability of resistance development when fungicides are employed.

In Spain, management of the cucurbit powdery mildew pathogen Podosphaera xanthii is strongly dependent on chemicals such as quinone outside inhibitor (QoI) fungicides. In a previous report, widespread resistance to QoI fungicides in populations of P. xanthii in south-central Spain was documented, but the molecular mechanisms of resistance remained unclear. In this work, the role of the Rieske-FeS (risp) and the cytochrome b (cytb) gene mutations in QoI resistance of P. xanthii were examined. No point mutations in the risp gene were found in the three QoI-resistant isolates analyzed. For cytb, sequence analysis revealed the presence of a G143A substitution that occurs in many QoI-resistant fungi. This mutation was always detected in QoI-resistant isolates of P. xanthii; however, it was also detected in sensitive isolates. To better understand the role of heteroplasmy for cytb in QoI resistance of P. xanthii, an allele-specific quantitative PCR was developed to quantify the relative abundance of the G143 (sensitive) and A143 (resistant) alleles. High relative abundance of A143 allele (70%) was associated with isolates resistant to QoI fungicides; however, QoI-sensitive isolates also carried the mutated allele in frequencies ranged from 10 to 60%. Our data suggest that G143A mutation in cytb is the primary factor involved in QoI resistance of P. xanthii but the proportion of G143 and A143 alleles in an isolate may determine its QoI resistance level.