Poster
Fang Wei Yuen
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Markéta Vlková
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Catrin Weiler
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Daria Evseeva
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Rekha Gopalan-Nair
Postdoctoral researcher
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Hongwen Huang
Chinese Academy of Sciences
Guangzhou, Guangdong, China (People's Republic)
Young Jin Koh
Sunchon National University
Suncheon, Kangwon-do, Republic of Korea
Kee Hoon Sohn, PhD (he/him/his)
Associate Professor
Seoul National University
Seoul, Seoul-t'ukpyolsi, Republic of Korea
Yuichi Takikawa
Shizuoka University
Shizuoka, Shizuoka, Japan
Honour McCann
Max Planck Institute for Biology
Tübingen, Baden-Wurttemberg, Germany
Paul Rainey
Max Planck Institute
Plön, Schleswig-Holstein, Germany
Elena Colombi
Macquarie University
Sydney, New South Wales, Australia
Christina Straub
Universität Wien
Wien, Wien, Austria
The risk of the emergence and rapid spread of novel diseases is increased by the intensive cultivation of clonally propagated crop plants. Pseudomonas syringae pv. actinidiae (Psa) was first identified as the causal agent of kiwifruit (Actinidia chinensis) canker disease in the mid-1980s. In 2008, a new lineage emerged to cause a global outbreak. My analysis of a 2,200-isolate collection of Pseudomonas from kiwifruit shows distantly related P.savastanoi are frequently recovered from Actinidia spp., in both wild and cultivated hosts, Psa-infected and uninfected alike. Psa and P. savastanoi thus evolved separately to colonise the same host, but with different infection outcomes. I am investigating whether Psa and P. savastanoi share specific strategies, such as effectors or toxins that allow them to subvert host immune responses and whether this variation in their ability to infect the same host is linked with their carriage of specific effectors or effector alleles. I will highlight my analysis of the mobile elements circulating between these species, and the type 3 secreted effectors that may act as molecular drivers of plant-microbe coevolutionary interactions. This study aims to shed light on the adaptive strategies employed by pathogens and potentially help mitigate devastating outbreaks in the future.