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The genome of the grape powdery mildew pathogen

ABSTRACT: Powdery mildew (Erysiphe necator) is a widespread and economically important disease of grapevines. Large quantities of fungicides are used for its control, accelerating the incidence of fungicide-resistance. A shotgun approach was applied to sequence and assemble the E. necator genome of five isolates, and RNA-seq and comparative genomics were used to predict and annotate protein-coding genes. In addition, a collection of 98 E. necator isolates collected from diverse locations was used for SSR profiling and was screened for copy number variation and presence/absence of a single point mutation (Y136F) in the CYP51 gene, a key target for DMI fungicides. Our results show that the E. necator genome is exceptionally large and repetitive and suggests that transposable elements are responsible for genome expansion. Frequent structural variations were found between isolates and included copy number variant (CNV) in CYP51. We show that CYP51 copy number correlates with expression level and that an increase in copy number is detected in isolates collected from fungicide-treated vineyards. This copy number variation was usually detected with the CYP51 mutant allele (Y136F), suggesting that an increase in copy number becomes advantageous only when the allele is mutated. We also show that CYP51 copy number correlates with fungal growth in the presence of DMI fungicide in vitro. These results suggest that copy number variation can be adaptive in the development of resistance to DMI fungicides in E. necator.

ORGANISM(S): Vitis vinifera

PROVIDER: GSE58958 | GEO | 2014/12/10

SECONDARY ACCESSION(S): PRJNA254035

REPOSITORIES: GEO

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The genome of the grape powdery mildew pathogen

Project description:Powdery mildew (Erysiphe necator) is a widespread and economically important disease of grapevines. Large quantities of fungicides are used for its control, accelerating the incidence of fungicide-resistance. A shotgun approach was applied to sequence and assemble the E. necator genome of five isolates, and RNA-seq and comparative genomics were used to predict and annotate protein-coding genes. In addition, a collection of 98 E. necator isolates collected from diverse locations was used for SSR profiling and was screened for copy number variation and presence/absence of a single point mutation (Y136F) in the CYP51 gene, a key target for DMI fungicides. Our results show that the E. necator genome is exceptionally large and repetitive and suggests that transposable elements are responsible for genome expansion. Frequent structural variations were found between isolates and included copy number variant (CNV) in CYP51. We show that CYP51 copy number correlates with expression level and that an increase in copy number is detected in isolates collected from fungicide-treated vineyards. This copy number variation was usually detected with the CYP51 mutant allele (Y136F), suggesting that an increase in copy number becomes advantageous only when the allele is mutated. We also show that CYP51 copy number correlates with fungal growth in the presence of DMI fungicide in vitro. These results suggest that copy number variation can be adaptive in the development of resistance to DMI fungicides in E. necator. Detach Carignan leaves were sprayed with a Erysiphe necator C-strain conida suspension, leaves were collected in 4 time points (12 hours, 24 hours, 3 days, and 6 days) post inoculation. For each time point, two leaves from the same seedling were pooled and frozen in liquid nitrogen, and each time point was performed in triplicate.

2014-12-10 | E-GEOD-58958 | biostudies-arrayexpress

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Project description:Background: Copy number variation is an important component of genetic variation in higher eukaryotes. The extent of natural copy number variation in C. elegans is unknown outside of 2 highly divergent wild isolates and the canonical N2 Bristol strain. Results: We have used array comparative genomic hybridization (aCGH) to detect copy number variation in the genomes of 12 natural isolates of Caenorhabditis elegans. Deletions relative to the canonical N2 strain are more common in these isolates than duplications, and indels are enriched in multigene families on the autosome arms. Among the strains in our study, the Hawaiian and Madeiran strains (CB4856 and JU258) carry the largest number of deletions, followed by the Vancouver strain (KR314). Overall we detected 510 different deletions affecting 1136 genes, or over 5% of the genes in the canonical N2 genome. The indels we identified had a median length of 2.7 kb. Since many deletions are found in multiple isolates, deletion loci were used as markers to derive an unrooted tree to estimate genetic relatedness among the strains. Conclusion: Copy number variation is extensive in C. elegans, affecting over 5% of the genes in the genome. The deletions we have detected in natural isolates of C. elegans contribute significantly to the number of deletion alleles available to researchers. The relationships between strains are complex and different regions of the genome possess different genealogies due to recombination throughout the natural history of the species, which may not be apparent in studies utilizing smaller numbers of genetic markers.

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Searching for the mechanism that mediates mefenoxam-acquired resistance in Phytophthora infestans and how it is regulated

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