Plant pathogens are a persistent agricultural problem that cause billions of dollars in losses annually. As global nutritional needs increase with a growing population, it is critical to gain a better understanding of the molecular mechanisms underlying plant-pathogen interactions, to reduce crop losses from disease. The bacterial plant pathogen Pseudomonas syringae pv. tomato (Pst) utilizes a needle-like structure called the type III secretion system (T3SS) to deliver entire suites of proteins, called effectors, directly into the plant cell. These type III-secreted effectors (T3SEs) suppress plant immunity and promote pathogen virulence. However, plants have evolved to recognize T3SEs and trigger defense responses in a process called effector-triggered immunity (ETI). The work herein aims to further elucidate the complex co-evolutionary relationship between Pst and its hosts, and utilizes the wild tomato species Solanum pimpinellifolium as a genetic resource for the discovery of novel immune elicitors in the Pst-tomato pathosystem. Chapter 1 introduces the plant immune system and the current use of wild species in identifying sources of disease resistance. In Chapter 2, I present the protocol for a high-throughput seedling-based assay which allows for the rapid screening of tomato for resistance to various bacterial plant pathogens. This approach enables for larger sample size, decreased space requirements, and shorter timeframes than previously used approaches using adult plants. An application for the seedling flood assay is found in Chapter 3, which identifies the S. pimpinellifolium accession LA1987 as resistant to the emerging pathogen Pst T1. We then utilized 2 virulent strains of P. syringae to deliver candidate PstT1 T3SEs to LA1987 and screen for a gain of resistance and found that multiple PstT1 T3SEs were capable of eliciting ETI in LA1987. Interestingly we also found that ETI elicitation by a T3SE could vary based on the strain delivering the effector. A closer examination of the strains used revealed distinct effector suites, suggesting T3SEs encoded by the delivering pathogen may suppress ETI elicitation. Together, these results indicate a role for metaeffector interactions in determining immunity elicitation and underline their importance in understanding plant-pathogen interactions. In Chapter 4, we provide a further examination of the roles of T3SEs in suppressing immunity and promoting pathogen fitness. We present a comprehensive review of T3SEs from multiple bacterial plant pathogens and discuss their activation, modes of action, and targets in planta. Chapter 5 describes a minimal CRISPR-Cas3 which is a promising tool for the future characterization of effector function in bacterial pathogens. This system is capable of making large-scale deletions and can therefore be used to delete multiple T3SEs, encoded on genomic clusters, at once. I provide proof-of-principle for the use of the minimal CRISPR-Cas3 system to generate effector polymutants in the model pathogen Pst DC3000. Effector polymutants generated with CRISPR-Cas3 performed similarly in vitro and in planta to previously made polymutants, and allowed for the characterization of effector cluster function during infection of the model plant Arabidopsis thaliana. These data provide support for the use of CRISPR-Cas3 to more rapidly generate effector polymutants in diverse hosts. Finally, in Chapter 6, I describe the characterization of a novel resistance mechanism deployed by S. pimpinellifolium to a PstDC3000 effector polymutant. The effectorless mutant of PstDC3000 has been deleted for all 36 of its putative T3SEs, but still possesses a fully functional T3SS. We found that even in the absence of effectors, this strain was capable of eliciting a hypersensitive response (HR), a hallmark of ETI, in several accessions of S. pimpinellifolium. The HR appears to be dependent on a functional T3SS, but is not dependent on effector delivery, indicating S. pimpinellifolium may recognize a component of the T3SS machinery to trigger immunity. Though this phenomenon has been observed in animal systems, it has not previously been observed in plants. We observed that this T3SS-triggered immune response is rarely observed in cultivated tomato, and that it can be suppressed by delivered T3SEs, highlighting the importance of both effector polymutants and wild species in the discovery of this resistance complex. Taken together, this work identifies several roles for the T3SS in determining pathogen outcomes in planta. We provide evidence for both the elicitation and suppression of immunity by T3SEs and additionally suggest a new mechanism for pathogen recognition in which the T3SS machinery itself is recognized to trigger immunity. These results not only elucidate the co-evolutionary relationship between Pst and tomato, but also provide new targets for the breeding of disease-resistant crops.