The role of defense signaling pathways in the interaction of Arabidopsis thaliana and Vertcillium longisporum

Verticillium longisporum is a soil-borne fungal pathogen causing vascular disease predominantly in oilseed rape. The pathogen enters its host through the roots and maintains a parasitic life stage in the xylem before invading other tissues late in the infection cycle. Arabidopsis thaliana was used as a model plant to characterize the response of the aerial parts of the plants towards this pathogen. It was shown that V. longisporum infections lead to increased amounts of salicylic acid metabolites, jasmonic acid-isoleucine and abscisic acid in the petioles of infected Arabidopsis plants at 15 dpi. Infection of salicylic acid biosynthesis and signaling mutants resulted in similar disease phenotype as in the wild type depicting a weak role of salicylic acid in V. longisporum/Arabidopsis interaction. It was found that the jasmonic acid/ethylene pathway was not as highly activated as by the necrotrophic pathogen Botrytis cinereae, whereas the jasmonic acid pathway was as efficiently induced as after wounding. Infection of the jasmonic acid receptor mutant, coi1, led to reduced disease symptoms towards V. longisporum as compared to the corresponding wild type and the jasmonic acid biosynthesis mutant dde2-2. Initial colonization of the roots was comparable in wild type and coi1 plants and similar amounts of fungal biomass were accumulated in petioles of both genotypes at 10 dpi. It was shown that COI1 acts independently of any JA-Ile or JA-Ile mimics. Whole genome microarray experiments using petioles of wild type, dde2-2 and coi1-t plants at 15 dpi did not reveal over/under- representation of any known defense pathways in coi1-t plants that might lead to the resistance phenotype. However, genes related to cell wall processes were over-represented in the cluster of genes that were induced to a similar extent in all three genotypes. Assessment of V. longisporum-induced alterations of the vascular bundles revealed that the de-differentiation process is visible in the wild type petioles at 10 dpi and appeared to be less pronounced in the resistant coi1-t plants. Grafting studies revealed that impaired shoot growth and early senescence was dependent on a functional COI1 allele in the roots, whereas COI1 in the shoots was not necessary for a visible phenotype (Ralhan et al., 2012). Since V. longisporum infection does not lead to the clogging of the vessel (Floerl et al., 2008, 2010), a mobile signal generated in the roots has been postulated that might be responsible for the induction of the disease symptoms in the shoots