Comparative genomics of Pseudomonas syringae reveals convergent gene gain and loss associated with specialization onto cherry (Prunus avium). Issue 2 (4th May 2018)

• Record Type: Journal Article
• Authors: Hulin, Michelle T.; Armitage, Andrew D.; Vicente, Joana G.; Holub, Eric B.; Baxter, Laura; Bates, Helen J.; Mansfield, John W.; Jackson, Robert W.; Harrison, Richard J.
• Is Part Of: New phytologist. Volume 219:Issue 2(2018)
• Page Start: 672
• Page End: 696
• Publication Date: 2018-05-04
• Subjects: avirulence -- bacterial canker -- comparative genomics -- host specialization -- prediction -- Pseudomonas -- toxins -- type III effectors; Botany -- Periodicals; 580
• DOI: 10.1111/nph.15182
• Languages: English
• ISSNs: 0028-646X

Abstract

Summary: Genome‐wide analyses of the effector‐ and toxin‐encoding genes were used to examine the phylogenetics and evolution of pathogenicity amongst diverse strains of Pseudomonas syringae causing bacterial canker of cherry ( Prunus avium ), including pathovars P. syringae pv morsprunorum ( Psm ) races 1 and 2, P. syringae pv syringae ( Pss ) and P. syringae pv avii . Phylogenetic analyses revealed Psm races and P. syringae pv avii clades were distinct and were each monophyletic, whereas cherry‐pathogenic strains of Pss were interspersed amongst strains from other host species. A maximum likelihood approach was used to predict effectors associated with pathogenicity on cherry. Pss possesses a smaller repertoire of type III effectors but has more toxin biosynthesis clusters than Psm and P. syringae pv avii . Evolution of cherry pathogenicity was correlated with gain of genes such as hopAR1 and hopBB1 through putative phage transfer and horizontal transfer respectively. By contrast, loss of the avrPto/hopAB redundant effector group was observed in cherry‐pathogenic clades. Ectopic expression of hopAB and hopC1 triggered the hypersensitive reaction in cherry leaves, confirming computational predictions. Cherry canker provides a fascinating example of convergent evolution of pathogenicity that is explained by the mix of effector and toxin repertoires acting on a common host. Abstract : See also the Commentary on this article byBaltrus & Orth, 219 : 482–484 .