Transposition, insertion, deletion and recombination drive variability in the type 3 secretome of pseudomonas syringae pv. Actinidiae, the transition from global effector comparisons to kiwifruit resistance breeding strategies

A strain of Pseudomonas syringae pv. actinidiae (Psa) that is particularly virulent (Psa-V or biovar 3) is responsible for the recent devastating global outbreak of bacterial canker on kiwifruit vines. We have now sequenced the genomes of over 30 isolates of Psa from around the world including two genomes (Psa-V and the type strain) to near completion. This extensive resource of genomic information has allowed us to reveal the remarkable plasticity exhibited by this pathogen and trace its evolution from the first geographically limited outbreaks on commercial kiwifruit production in the 1980s to the present global outbreak. We present examples of how this plasticity is driven by several different mechanisms including transposition, insertions/deletions and genome level recombination events and has resulted in at least four major phylogenetically defined groupings of Psa strains. These mechanisms have scrambled long distance co-linearity between even the most closely related of these phylogenetic groups, underlining the pace of genome-wide evolution in P. syringae pathovars. We focus on the impact of these events on the effector complement of the four main groupings of Psa strains in particular. As the loss of host resistance is typically linked with loss of these effectors we discuss how this knowledge is now being used to inform the long-term resistance breeding strategies being developed against this very damaging pathogen