| Plants utilize an array of complex mechanisms to resist pathogens, After initial recognition of the pathogen, subsequent signaling events culminate in resistance. The nature of these signaling events is poorly understood, although several mutants have been identified that appear to be compromised in signaling. In this thesis, I describe characterization of the pbs2-1 mutant of Arabidopsis, which displays increased susceptibility to multiple pathogens. I cloned PBS2 and demonstrated that it is equivalent to the Rar1 gene of barley, which is required for resistance to powdery mildew disease. Analysis of PBS2 indicated that it is required for the stability of disease resistance proteins that mediate pathogen recognition. Therefore, PBS2 functions at the level of pathogen recognition, rather than in a downstream signaling pathway.; To better understand plant resistance signaling, I analyzed the Pseudomonas syringae AvrPphB protein and demonstrated that it belongs to the CA clan of papain-like cysteine proteases. Protease activity is required for elicitation of host responses, indicating that AvrPphB is recognized via its enzymatic activity, rather than by direct binding to a host cell receptor. I also showed that AvrPpiC2, a homolog of AvrPphB found in P. syringae strain DC3000, contributes to virulence on Arabidopsis and elicits defense responses on bean plants. These data indicate that plants may typically recognize pathogens by detecting the enzymatic activities of their virulence proteins. |