Genomic Variation and Host Interaction among Pseudomonas syringae pv. actinidiae Strains in Actinidia chinensis 'Hongyang'.

Kiwifruit bacterial canker is a recent epidemic disease caused by Pseudomonas syringae pv. actinidiae ( Psa ), which has undergone worldwide expansion in a short time and resulted in significant economic losses. 'Hongyang' ( Actinidia chinensis ), a widely grown cultivar because of its health-beneficial nutrients and appreciated red-centered inner pericarp, is highly sensitive to Psa . In this work, ten Psa strains were isolated from 'Hongyang' and sequenced for genome analysis. The results indicated divergences in pathogenicity and pathogenic-related genes among the Psa strains. Significantly, the interruption at the 596 bp of HrpR in two low-pathogenicity strains reemphasized this gene, expressing a transcriptional regulator for the effector secretion system, as an important pathogenicity-associated locus of Psa . The transcriptome analysis of 'Hongyang' infected with different Psa strains was performed by RNA-seq of stem tissues locally (at the inoculation site) and systemically. Psa infection re-programmed the host genes expression, and the susceptibility to Psa might be attributed to the down-regulation of several genes involved in plant-pathogen interactions, especially calcium signaling transduction, as well as fatty acid elongation. This suppression was found in both low- and high-pathogenicity Psa inoculated tissues, but the effect was stronger with more virulent strains. Taken together, the divergences of P. syringae pv. actinidiae in pathogenicity, genome, and resulting transcriptomic response of A . chinensis provide insights into unraveling the molecular mechanism of Psa -kiwifruit interactions and resistance improvement in the kiwifruit crop.