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Cherry canker genetics - applying genomics to the control of perennial disease problems in fruit trees

Michelle Hulin: NIAB EMR

<div></p> <p><em>Pseudomonas syringae</em> pathovars are highly specialised, with individual strains only infecting one or a few hosts. It is believed this host specificity is due to the repertoire of type III effector proteins involved in both virulence and avirulence <em>in planta</em>. This topic was explored using comparative genomics of three divergent clades that have convergently evolved to cause bacterial canker on cherry (<em>Prunus avium</em>). The clades include <em>P. syringae </em>pv. <em>morsprunorum </em>(<em>Psm</em>) races 1 and 2 (which are now known to be distantly related) and <em>P. syringae </em>pv. <em>syringae </em>(<em>Pss</em>). Three reference isolates of <em>Psm</em> R1, R2 and <em>Pss</em> were sequenced with PacBio and the genomes of a diverse set of further strains were sequenced using the Illumina MiSeq. Genomic analysis of the <em>Prunus</em> strains has revealed highly divergent effector and toxin repertoires within and between the different clades, indicating they use distinct mechanisms to cause bacterial canker. A bayesian approach was utilised to predict effectors whose evolution is significantly associated with the evolution of pathogenicity for cherry. Candidate virulence effectors have been gained via horizontal gene transfer which has been both plasmid and phage mediated. By contrast, the HopAB effector family has been lost or truncated in cherry-pathogenic clades. Members of this effector family were cloned and ectopically expressed in pathogenic strains and found to trigger immunity, leading to avirulence on cherry leaves. Work is now underway to identify the role of conserved effectors in virulence. This is in parallel with work on the host looking for both effector-driven and more quantitative host resistance mechanisms.</div>

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