Arabidopsis-Verticillium interaction as a model disease system

Most of our understanding of plant defense against pathogens has come from studies with microorganisms causing foliar diseases. To contribute to the elucidation of the molecular genetics of host resistance against systemic invaders, we are studying the interaction of the model plant Arabidopsis thaliana with the soil-borne fungus Verticillium longisporum, causal agent of vascular diseases of cruciferous and non-cruciferous crops worldwide. We have found that in Arabidopsis, like in other plant species, V. longisporum infection induces disease symptoms by interfering with the host developmental program. In particular, the pathogen causes early flowering, accelerated senescence and rapid death in the susceptible accession Columbia, whereas, it extends vegetative growth and causes only mild chlorosis in the more tolerant accession C-24. Via forward genetics, we isolated mutants of C-24 with altered disease phenotype and identified three independent loci, VERTCILLIUM HYPERSENSITIVE (VHS) 1 to 3, able to convey increased tolerance likely functioning as negative regulators of the pathogen-induced transition to flowering and/or senescence syndrome. The vhs3 mutation was linked to disruption of AtBRM, coding a SNF2 chromatin remodeling protein. We will present data characterizing pleiotropic effects of vhs mutations on Arabidopsis defense responses and development. Furthermore, we will discuss results from genome-wide transcriptional analysis upon pathogen challenge, providing new insights on signaling pathways controlling basal defense mechanisms.