Abstract
Pseudomonas syringae pv. actinidiae (Psa) biovar 3 caused pandemic bacterial canker of Actinidia chinensis and Actinidia deliciosa since 2008. In Europe, the disease spread rapidly in the kiwifruit cultivation areas from a single introduction. In this study, we investigated the genomic diversity of Psa biovar 3 strains during the primary clonal expansion in Europe using single molecule real-time (SMRT), Illumina and Sanger sequencing technologies. We recorded evidences of frequent mobilization and loss of transposon Tn6212, large chromosome inversions, and ectopic integration of IS sequences (remarkably ISPsy31, ISPsy36, and ISPsy37). While no phenotype change associated with Tn6212 mobilization could be detected, strains CRAFRU 12.29 and CRAFRU 12.50 did not elicit the hypersensitivity response (HR) on tobacco and eggplant leaves and were limited in their growth in kiwifruit leaves due to insertion of ISPsy31 and ISPsy36 in the hrpS and hrpR genes, respectively, interrupting the hrp cluster. Both strains had been isolated from symptomatic plants, suggesting coexistence of variant strains with reduced virulence together with virulent strains in mixed populations. The structural differences caused by rearrangements of self-genetic elements within European and New Zealand strains were comparable in number and type to those occurring among the European strains, in contrast with the significant difference in terms of nucleotide polymorphisms. We hypothesize a relaxation, during clonal expansion, of the selection limiting the accumulation of deleterious mutations associated with genome structural variation due to transposition of mobile elements. This consideration may be relevant when evaluating strategies to be adopted for epidemics management.
Highlights
Pseudomonas syringae pv. actinidiae (Psa) is the causal agent of bacterial canker of green-fleshed (Actinidia deliciosa) and yellow-fleshed kiwifruit (Actinidia chinensis) (Scortichini et al, 2012)
Psa biovar 3 strains isolated in different regions of Europe were investigated to assess their phytopathogenic and genomic diversity
As expected, induced hypersensitivity response (HR) in eggplant and tobacco leaves when infiltrated at concentrations of 1–2 × 108 CFU/ml, strains CRAFRU 12.50 and CRAFRU 12.29 failed in eliciting HR
Summary
Pseudomonas syringae pv. actinidiae (Psa) is the causal agent of bacterial canker of green-fleshed (Actinidia deliciosa) and yellow-fleshed kiwifruit (Actinidia chinensis) (Scortichini et al, 2012). 2008–2011, sudden and repeated epidemics of bacterial canker developed firstly in central Italy (Balestra et al, 2009; Ferrante and Scortichini, 2009, 2010), and, subsequently, in all the other major areas of kiwifruit cultivation such as New Zealand (Everett et al, 2011), and Chile (EPPO, 2016). Genomic and genetic analyses have soon revealed that the Psa strains causing the 2008–2011 epidemics differed significantly from those previously found in Italy (Marcelletti et al, 2011) and that the first outbreaks of kiwifruit bacterial canker in Italy (Ferrante et al, 2015) were caused by a rapid and clonal expansion of the pathogen in the cultivated areas (Marcelletti and Scortichini, 2011). The availability of strains isolated in China, the area of origin of many Actinidia spp., and the intensive use of Illumina sequencing of bacterial genomes (Mazzaglia et al, 2012; Butler et al, 2013; McCann et al, 2013, 2017) and VNTR analysis (Cesbron et al, 2015; Ciarroni et al, 2015; Cunty et al, 2015a) paved the way to the understanding of the epidemiology of this important disease
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