Reconstitution of a model plant disease 
X. XIN (1), K. Nomura (1), K. Aung (1), A. Velásquez (1), J. Yao (1), F. Boutrot (2), C. Zipfel (2), J. Chang (3), S. He (1) (1) Michigan State University, U.S.A.; (2) The Sainsbury Laboratory, United Kingdom; (3) Oregon State University, U.S.A.

The Arabidopsis-Pseudomonas syringae pathosystem has been widely used for understanding bacterial pathogenesis and disease susceptibility in plants, leading to influential models that depict immune suppression mediated by type III effectors as a key step of bacterial pathogenesis. Here, disease reconstitution experiments showed that immune suppression is insufficient for P. syringae pathogenesis in Arabidopsis. Instead, humidity-dependent, pathogen-driven formation of aqueous apoplast was found to be another critical step. Two conserved effectors from P. syringae, HopM1 and AvrE, are sufficient and necessary to produce aqueous apoplast in the context of bacterial infection. Remarkably, HopM1 is also sufficient to transform non-pathogenic P. syringae strains into virulent pathogens in Arabidopsis that is deficient in pattern-triggered immunity (PTI), but not in plants defective in salicylic acid signaling. Likewise, Arabidopsis quadruple mutants that are simultaneously defective in PTI and a host target of HopM1 could substantially rescue the basic features of this model disease and, interestingly, lose control of the endogenous leaf “bacteriome”. Thus, we have defined the minimal host processes underlying foliar bacterial pathogenesis and bacteriome homeostasis in a model plant. Results provide a new framework for pathogenesis and microbiome studies in plants.

Abstract Number: P9-324
Session Type: Poster