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Background  Hazelnut ( Corylus avellana ) decline disease in Greece and Italy is caused by the convergent evolution of two distantly related lineages of  Pseudomonas syringae  pv.  avellanae  ( Pav ). We sequenced the genomes of three  Pav  isolates to determine if their convergent virulence phenotype had a common genetic basis due to either genetic exchange between lineages or parallel evolution.    Results  We found little evidence for horizontal transfer (recombination) of genes between  Pav  lineages, but two large genomic islands (GIs) have been recently acquired by one of the lineages. Evolutionary analyses of the genes encoding type III secreted effectors (T3SEs) that are translocated into host cells and are important for both suppressing and eliciting defense responses show that the two  Pav  lineages have dramatically different T3SE profiles, with only two shared putatively functional T3SEs. One  Pav  lineage has undergone unprecedented secretome remodeling, including the acquisition of eleven new T3SEs and the loss or pseudogenization of 15, including five of the six core T3SE families that are present in the other  Pav  lineage. Molecular dating indicates that divergence within both of the  Pav  lineages predates their observation in the field. This suggest that both  Pav  lineages have been cryptically infecting hazelnut trees or wild relatives for many years, and that the emergence of hazelnut decline in the 1970s may have been due to changes in agricultural practice.    Conclusions  These data show that divergent lineages of  P. syringae  can converge on identical disease etiology on the same host plant using different virulence mechanisms and that dramatic shifts in the arsenal of T3SEs can accompany disease emergence.

Extensive remodeling of the Pseudomonas syringae pv. avellanae type III secretome associated with two independent host shifts onto hazelnut