Adaptive genomic structural variation in the grape powdery mildew pathogen, Erysiphe necator

Abstract

BackgroundPowdery mildew, caused by the obligate biotrophic fungus Erysiphe necator, is an economically important disease of grapevines worldwide. Large quantities of fungicides are used for its control, accelerating the incidence of fungicide-resistance. Copy number variations (CNVs) are unbalanced changes in the structure of the genome that have been associated with complex traits. In addition to providing the first description of the large and highly repetitive genome of E. necator, this study describes the impact of genomic structural variation on fungicide resistance in Erysiphe necator.ResultsA shotgun approach was applied to sequence and assemble the genome of five E. necator isolates, and RNA-seq and comparative genomics were used to predict and annotate protein-coding genes. Our results show that the E. necator genome is exceptionally large and repetitive and suggest that transposable elements are responsible for genome expansion. Frequent structural variations were found between isolates and included copy number variation in EnCYP51, the target of the commonly used sterol demethylase inhibitor (DMI) fungicides. A panel of 89 additional E. necator isolates collected from diverse vineyard sites was screened for copy number variation in the EnCYP51 gene and for presence/absence of a point mutation (Y136F) known to result in higher fungicide tolerance. We show that an increase in EnCYP51 copy number is significantly more likely to be detected in isolates collected from fungicide-treated vineyards. Increased EnCYP51 copy numbers were detected with the Y136F allele, suggesting that an increase in copy number becomes advantageous only after the fungicide-tolerant allele is acquired. We also show that EnCYP51 copy number influences expression in a gene-dose dependent manner and correlates with fungal growth in the presence of a DMI fungicide.ConclusionsTaken together our results show that CNV can be adaptive in the development of resistance to fungicides by providing increasing quantitative protection in a gene-dosage dependent manner. The results of this work not only demonstrate the effectiveness of using genomics to dissect complex traits in organisms with very limited molecular information, but also may have broader implications for understanding genomic dynamics in response to strong selective pressure in other pathogens with similar genome architectures.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-1081) contains supplementary material, which is available to authorized users.

Exploring the genomic diversity of black yeasts and relatives (Chaetothyriales,Ascomycota)

“…S6). The important Y136F mutation (Mullins et al., 2011, Jones et al., 2014a) associated with CYP51 copy number variation and involved in azole resistance was not identified in these genes. This suggests that the tolerant allele, responsible for the azole resistance, is acquired only in the presence of azole fungicides.…”

Prevalence of Major Methicillin-Resistant Staphylococcus aureus Clones in Korea Between 2001 and 2008

“…The most common lineages in the USA are CC1 (USA400) and CC8 (USA300), which usually carry SCC mec type IV and PVL-encoding genes and are becoming the subject of intense research [315]. The four PVL-positive MRSA stains in this study had ST30 (one isolate) or ST8 (three isolates) characteristics.…”

PCR Multiplexes DiscriminateFusariumSymbionts of InvasiveEuwallaceaAmbrosia Beetles that Inflict Damage on Numerous Tree Species Throughout the United States

“…Whole-genome sequences of closely related fungal species has provided new insight into many other economically important fungal pathogens (Jones et al 2014;Schmidt et al 2016), including other fusaria (Maphosa et al 2016). This diagnostic tool can easily be expanded in the event that other AFC-Euwallacea mutualists are introduced into the United States.…”