Effector knockout competition reveals individually redundant effectors are collectively required for successful virulence
Abstract
The 2010 incursion of Pseudomonas syringae pv. actinidiae (Psa) in New Zealand devastated susceptible kiwifruit orchards. The kiwifruit industry has since recovered following the deployment of more tolerant cultivars. However, little is known about the extent to which the Psa population is evolving in orchards and further adapting to its kiwifruit hosts. Effector proteins help pathogens invade their host, extract nutrients, and suppress immunity. Psa is an emergent kiwifruit pathogen with over thirty functional effectors, providing a unique opportunity to understand how host selection shapes pathogen evolution. In particular, we seek to understand whether Psa requires all of its effectors to cause disease. Recent research suggests that only a few Psa effectors are required for virulence. Further still, resistant kiwifruit hosts such as Actinidia arguta can recognise several Psa effectors. Why, then, does Psa retain so many effectors in its repertoire? Using complementary approaches of orchard-based genome biosurveillance and effector knockout strain competition, we seek to examine effector requirements, redundancies, and repertoire refinement across different kiwifruit hosts. The selective pressure exerted by serially passaging a competitive pool of effector knockout strains in planta has allowed us to detect subtle contributions of effectors to virulence. While the majority of Psa’s effectors previously appeared to be non-essential, competition results suggest they may be collectively required for successful virulence. Competition has also revealed new host-specific effector requirements. This research provides important insights into the evolution of emergent pathogens and will ultimately ensure future resistance breeding efforts are robust and sustainable.
