P-046 - Immunity triggered by multiple effectors is required for nonhost resistance to Pseudomonas syringae pv. tomato DC3000 in Solanum americanum

Plants have evolved defense mechanisms against pathogens. Bacterial pathogens evade basal immunity by secreting effectors into the plant cells. In response, plants have evolved effector-triggered immunity (ETI) by immune receptor recognizing specific effectors, leading to hypersensitive response (HR) and bacterial growth restriction. Understanding ETI is crucial for developing disease-resistant crops. Wild plant species are valuable sources of resistance genes. Solanum americanum, a wild Solanaceae species, has been used to identify NLR genes. Genetic diversity and a well-sequenced genome make it an ideal model plant for NLR gene discovery. In this study, we aim to understand the genetic basis of S. americanum resistance against the model bacterial pathogen Pto DC3000. We identified multiple Pto DC3000 effectors (AvrPto, HopAD1, HopAM1, HopC1, HopAA1-1, HopM1, and AvrE1) triggering HR in S. americanum. We then generated Pto DC3000 mutants lacking HR-triggering effectors. Deletion of specific effectors enhanced bacterial growth and caused bacterial speck-like symptoms. Furthermore, the removal of all seven effectors abolished HR. In this study, we propose that multiple effectors are required for nonhost resistance in S. americanum and establish it as a model Solanaceae plant by enabling bacterial growth assay. Additionally, this system can help the identification of effector-recognizing resistance genes for developing durable disease resistance in Solanaceae crops.