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Extensive remodeling of the Pseudomonas syringae pv. avellanae type... » Isaúde
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BMC microbiology [electronic resource]
2012-07-17 03:29:06

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

Descrição: Background:Hazelnut (Corylus avellana) decline disease in Greece and Italy is caused by the convergentevolution of two distantly related lineages of Pseudomonas syringae pv. avellanae (Pav). Wesequenced the genomes of three Pav isolates to determine if their convergent virulencephenotype had a common genetic basis due to either genetic exchange between lineages orparallel evolution.Results:We found little evidence for horizontal transfer (recombination) of genes between Pavlineages, but two large genomic islands (GIs) have been recently acquired by one of thelineages. Evolutionary analyses of the genes encoding type III secreted effectors (T3SEs) thatare translocated into host cells and are important for both suppressing and eliciting defenseresponses show that the two Pav lineages have dramatically different T3SE profiles, withonly two shared putatively functional T3SEs. One Pav lineage has undergone unprecedentedsecretome remodeling, including the acquisition of eleven new T3SEs and the loss orpseudogenization of 15, including five of the six core T3SE families that are present in theother Pav lineage. Molecular dating indicates that divergence within both of the Pav lineagespredates their observation in the field. This suggest that both Pav lineages have beencryptically infecting hazelnut trees or wild relatives for many years, and that the emergenceof 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 diseaseetiology on the same host plant using different virulence mechanisms and that dramatic shiftsin the arsenal of T3SEs can accompany disease emergence.

Identificador: doi:10.1186/1471-2180-12-141
Volume: 0
Página: 1 a


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