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

BMC Genomics

Dario Cantu¹  M Andrew Walker¹  W Douglas Gubler²  Brianna McGuire²  Katherine CH Amrine¹  Abraham Morales-Cruz¹  Summaira Riaz¹  Laura Jones¹ 

[1] Department of Viticulture and Enology, University of California Davis, One Shields Ave, Davis, CA 95616, USA;Department of Plant Pathology, University of California Davis, One Shields Ave, Davis, CA 95616, USA

关键词: CYP51;    Cytochrome p450;    Fungicide resistance;    Genetic adaptation;    Copy number variation;    Fungal genomics;   

Others  :  1127473
DOI  :  10.1186/1471-2164-15-1081

 received in 2014-08-02, accepted in 2014-12-01,  发布年份 2014

【 摘 要 】

Background

Powdery 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.

Results

A 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.

Conclusions

Taken 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.

【 授权许可】

   
2014 Jones et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.