Novel molecular mechanisms of disease susceptibility in plants -- an FTIR study of Arabidopsis thaliana

Understanding the molecular basis of plant resistance to fungal diseases will contribute to reducing world-wide crop losses. One model organism for studying disease resistance is Arabidopsis thaliana, a small member of the mustard family for which complete genomic sequence information was publicly released in 2000. Erysiphe cichoracearum, the causative agent for powdery mildew disease in a wide range of plants, colonizes and eventually overtakes a host if three events occur. Erysiphe spores are carried on the wind, and when they land on the aerial portions of a host plant, they must invade an epidermal (outer) cell, and establish a feeding structure to divert plant nutrients. The fungus must "fly under the radar" of the host's defense responses, which would, if fully activated, quickly kill the invading fungus. Finally, since the fungus is not a saprophytic pathogen (cannot survive on dead tissues), it must keep the host's cells alive until its life cycle is complete. Several genetic loci conferring powdery mildew resistance (pmr1-4) have previously been described by Vogel and Somerville [1]. While many disease-resistance pathways involve sensing of salicylic acid and/or jasmonic acid, several genes that operate independently of these hypersensitive responses have been identified; the mutant described below represents a novel form of disease resistance based upon loss of a gene required during a compatible interaction, rather than the action of known host defense pathways.