Host-pathogen interaction drives genome plasticity in the late blight pathogen

Phytophthora infestans causes late blight of potato and was the proximal cause of the Great Irish Famine. It remains a devastatingagricultural problem as it rapidly circumvents efforts at control by use of resistant cultivars and fungicides. The ~240 Mb genome of P. infestans is the largest and most complex in the chromalveolate lineage, and its sequence reveals features that illuminate its success as a pathogen. Comparison to other Phytophthora genomes shows massive expansion and a high rate of turnover in the content of genes encoding secreted proteins, including the host-translocated effectors of the RXLR class. P. infestans also has a vastly expanded array of Crinkler family genes. New functional analyses show that several classes of Crinklers trigger cell death when expressed inside plant cells, suggesting that they form a new class of host-translocated effectors. The genome structure itself likely plays a role in successful adaptation. The genome includes large repeat-rich regions where genes and gene order are not conserved. These regions are significantly enriched in rapidly evolving genes encoding secreted proteins such as RXLRs and Crinklers, and may provide a mechanism for easily duplicating successful effectors and deleting those that trigger resistance. For example, the Avr1 avirulence gene occurs at duplicated loci, and its avirulence allele is entirely absent in virulent strains. Sample sequencing of several strains of P. infestans and closely related Phytophthora species shows extensive copy number variation in the majority of secreted effectors, suggesting this as a common mechanism for evading resistance.