A Pathogenomic Approach to Decipher the Molecular Mechanisms Underlying Grapevine Diseases

Cultivated grapevines are susceptible to diseases caused by a broad spectrum of fungal pathogens. We have applied a shotgun approach to sequence the genomes of fungi associated with economically important diseases of grapevines, including the causal agents of powdery mildew (Erysiphe necator), Phomopsis cane and leafspot disease and Phomopsis dieback (Diaporthe ampelina), Botryosphaeria dieback (Neofusicoccum parvum and Botryosphaeria obtusa), Eutypa dieback (Eutypa lata), and Esca (Phaeomoniella chlamydospora and Togninia minima). We performed transcriptome profiling to characterize the transcriptional regulation of putative virulence factors, and to improve our protein-coding gene prediction pipeline. Whole genome re-sequencing provided us with information on the genetic diversity, both as sequence polymorphisms and structural variants, across fungal isolates collected from different hosts, with distinct aggressiveness on grapevines or tolerance to fungicides. As result, we identified families of genes potentially involved in processes associated with pathogenicity, such as degradation of particular cell wall components, polyketide toxin production, and necrosis induction. We employed a stochastic birth and death model to identify gene families that are significantly expanded in the genomes of the grapevine pathogens. To apply this model, we constructed a time-calibrated phylogenic tree of the fungal species, using a subset of conserved single-copy protein-coding genes and time of origin estimates from fossil records. We demonstrate that expanded gene families are significantly enriched in putative virulence factors suggesting that lineage-specific gene family expansions may have been adaptive in the evolution of grapevine pathogens.