The Gram-negative bacterial pathogen Pseudomonas syringae causes disease in diverse plant species, using the type III secretion system to inject type III secreted effector (T3SE) proteins into plant cells. T3SEs primarily function to suppress plant immunity. However plants can evolve NOD-like receptor (NLR) proteins that directly or indirectly recognize T3SEs. I will first discuss our work on the recognition of HopZ1a, an acetyltransferase that is part of the YopJ superfamily of T3SEs found in animal and plant pathogens. HopZ1a acetylates the pseudokinase ZED1, which triggers recognition by the NLR, ZAR1. ZED1 is proposed to act as a decoy, that traps the pathogen into revealing its presence to the host. ZAR1 has emerged as a key signaling hub in plant immunity, as it is also required for the recognition of multiple unrelated T3SE proteins from Xanthomonas campestris and P. syringae. We previously demonstrated that HopZ1a and ZED1 induce an immune response that is dependent on the ZAR1 homolog in N. benthamiana, indicating that ZAR1-mediated recognition is conserved from the Brassicaceae to the Solanaceae. Here, we performed a natural diversity screen in Arabidopsis and characterized polymorphic variants, to identify key molecular determinants of ZAR1-dependent immune induction. Second, I will discuss our work on the recognition of P. syringae in wild tomato. Emerging strains of P. syringae overwhelm genetic resistance that has been bred into common tomato cultivars. We previously developed a seedling-based flood assay to screen wild tomato accessions for resistance, and demonstrated that seedlings exhibit similar resistance or susceptibility phenotypes as adult plants. We have identified multiple wild accessions with resistance to P. syringae. I will discuss our progress in developing tools and identifying genetic factors in the host and pathogen that contribute to resistance.