The major focus of our research is to help understand, at molecular and cellular levels, how plants protect themselves against microbial pathogens. Two systems are being studied: 1)the response of tobacco to infection by tobacco mosaic virus (TMV), and 2)the interaction of Arabidopsis with turnip crinkle virus (TCV). Our major goal is to decipher the signal transduction pathway(s) which leads to induction of defense-related genes, such as the pathogenesis-related (PR) genes, that appear to underlie disease resistance. In particular, the role of salicylic acid (SA) in this pathway(s) is being studied. During the past several years, we have helped establish that a key component of this pathway is SA which can be reversibly inactivated and activated by conjugation and deconjugation to glucose, respectively. We have identified a putative receptor for SA; it is catalase. One of SA's mechanisms of action is to inhibit catalase's enzymatic activity, which results in elevated hydrogen peroxide levels. INA, a synthetic inducer of PR gene expression and enhanced disease resistance, also inhibits catalase activity. Moreover, SA and INA inhibit ascorbate peroxidase (APx), the other major enzyme for scavenging hydrogen peroxide.

The interaction of these two compounds with catalase and APx also appears to result in formation of SA and INA free radicals that give rise to lipid peroxides. These lipid peroxides activate PR genes. These two signal, elevated hydrogen peroxide levels and lipid peroxides, may act independently or in concert to induce PR-gene expression and enhanced disease resistance.