The research in my lab is aimed at expanding our basic understanding of the molecular mechanisms controlling programmed cell death (PCD) in plants. We have developed a pathogen-free model system based on the response of Arabidopsis thaliana to a purified fungal toxin, fumonisin B1 (FB1)
Two complementary strategies are being taken: 1) an Arabidopsis leaf mesophyll protoplast system to quantitatively examine PCD in defense-related mutants and to characterize the signal transduction pathway(s) controlling FB1-induced PCD; and 2) a genetic approach to identify Arabidopsis mutants resistant to FB1-induced PCD and/or affected in expression of ethylene- and jasmonate-dependent defense-related genes.
FB1 causes formation of necrotic lesions on Arabidopsis that resemble plant pathogen-induced lesions in many respects, including deposition of phenolic compounds and callose, accumulation of camalexin, production of reactive oxygen intermediates, and induction of pathogenesis-related (PR) gene expression. FB1-induced cell death in protoplasts is dependent on de novo transcription, translation, and reversible protein phosphorylation, confirming that FB1 elicits PCD in Arabidopsis. Roles for salicylic acid, ethylene and jasmonate in mediating FB1-induced PCD is supported by evaluation of FB1-induced cell death in defense-related Arabidopsis mutants and transgenic plants. To identify other factors contributing to FB1-induced PCD, Arabidopsis FB1-resistant (fbr) mutants were selected directly by sowing seeds on FB1-containing agar media.Further characterization of fbr mutants confirms that this high throughput mutant selection can reveal mutants with pathogen phenotypes. Moreover, the selection may also be useful in identifying components of developmental pathways.