Abstract
Verticillium longisporum is a soil-borne fungal pathogen that causes vascular disease predominantly in Brassicaceae. We have previously reported that the receptor of the plant defense hormone jasmonoyl-isoleucine (JA-Ile), CORONATINE INSENSITIVE 1 (COI1), is required in roots for the fungus to proliferate efficiently in the shoot, suggesting the presence of a mobile root-borne signal that influences the outcome of the disease in shoots. This function of COI1 in promoting susceptibility is independent of JA-Ile. To explore the underlying mechanisms, in this study we compared the root transcriptome of the Arabidopsis coi1 mutant with those of the susceptible JA-Ile-deficient allene oxide synthase (aos) mutant and the susceptible wild-type (WT). The biggest difference between the transcriptomes was due to 316 immunity-related genes that were constitutively higher expressed in coi1 as compared to the susceptible genotypes. Interfering with the expression of a sub-group of these genes partially suppressed the coi1-mediated tolerance phenotype. We therefore hypothesize that secreted defense compounds encoded by genes constitutively expressed in coi1 are transported to the shoot with the transpiration stream where they accumulate and interfere with fungal growth. In addition, we found that 149 of the 316 COI1-repressed genes were induced in the WT and aos upon infection, reaching similar expression levels as in mock-treated coi1. These were not further induced in coi1 upon infection. Thus, the repressive effect of COI1 is either lifted or overridden upon infection with V. longisporum.