CSIRO PUBLISHING www.publish.csiro.au/journals/app Australasian Plant Pathology, 2006, 35, 581–591 Salicylic acid mediates resistance to the vascular wilt pathogen Fusarium oxysporum in the model host Arabidopsis thaliana C. I. Edgar A,B , K. C. McGrath A,B,C , B. Dombrecht B , J. M. Manners A,B , D. C. Maclean A,B,C , P. M. Schenk A,D and K. Kazan A,B,E A Cooperative Research Centre for Tropical Plant Protection, The University of Queensland, John Hines Building Level 5, St Lucia, Qld 4072, Australia. B CSIRO Plant Industry, Queensland Bioscience Precinct, 306 Carmody Road, St Lucia, Qld 4067, Australia. C School of Molecular and Microbial Sciences, The University of Queensland, St Lucia, Qld 4072, Australia. D School of Integrative Biology, The University of Queensland, St Lucia, Qld 4072, Australia. E Corresponding author. Email: kemal.kazan@csiro.au Abstract. Fusarium oxysporum is a soilborne fungal pathogen that causes major economic losses by inducing necrosis and wilting symptoms in many crop plants. In this study, the interaction between F. oxysporum and the model plant Arabidopsis thaliana has been investigated to better understand the nature of host defences that are effective against the Fusarium wilt pathogen. The expression of salicylate- and jasmonate-responsive defence genes in F. oxysporum-challenged roots of A. thaliana plants as well as in the roots of plants whose leaves were treated with salicylate or jasmonate was analysed. Unexpectedly, genes (e.g. PR1, PDF1.2, and CHIB) encoding proteins with defensive functions or transcription factors (e.g. ERF1, AtERF2, AtERF4 and AtMYC2) known to positively or negatively regulate defences against F. oxysporum were not activated in F. oxysporum-inoculated roots. In contrast, the jasmonate-responsive defence gene PDF1.2 was induced in the leaves of plants whose roots were challenged with F. oxysporum, but the salicylate-responsive PR1 gene was not induced in the leaves of inoculated plants. Exogenous salicylic acid treatment prior to inoculation, however, activated PR1 and BGL2 defence gene expression in leaves and provided increased F. oxysporum resistance as evidenced by reduced foliar necrosis and plant death. Exogenous salicylic acid treatment of the foliar tissue did not activate defence gene expression in the roots of plants. This suggests that salicylate-dependent defences may function in foliar tissue to reduce the development of pathogen-induced wilting and necrosis. Despite the induction of defence gene expression in the leaves by jasmonate, this treatment did not lead to increased resistance to F. oxysporum. Overall, the results presented here suggest that the genetic manipulation of plant defence signalling pathways is a useful strategy to provide increased Fusarium wilt resistance. Introduction Plant pathogenic fungi can be roughly divided into two major groups, biotrophs and necrotrophs, based on their lifestyles on a given host species. Obligate biotrophs such as rust fungi require living host tissue to obtain nutrients and successfully complete their life cycles. In contrast, necrotrophic pathogens kill host cells (e.g. by secretion of toxins or cell wall degrading enzymes) and derive their nutrients from dead cells. Recently, significant progress has been made towards a better understanding of the basis of host resistance, particularly against biotrophic pathogens. A number of host genes (R-genes) conferring race-specific resistance to biotrophic pathogens have been cloned from various plant species. Proteins encoded by these resistance genes are involved in the direct or indirect recognition of pathogen signals generated during attempted infection. Pathogen recognition almost invariably leads to the activation of the plant’s defensive armoury, which may include the production of reactive oxygen, diverse secondary metabolites with antimicrobial activities, cell wall strengthening molecules and proteins that inhibit either microbial growth or microbial depolymerase enzymes. These defences are associated with the reprogramming of host gene expression and the hypersensitive response (HR), a form of programmed cell death. The HR is a very effective means of preventing infection by biotrophic pathogens. However, dead host cells resulting from a HR reaction can serve as potential starting points for infection by necrotrophs (Govrin and Levine 2000; Schenk et al. 2005). Another characteristic that broadly differentiates necrotrophs from biotrophs is that © Australasian Plant Pathology Society 2006 10.1071/AP06060 0815-3191/06/060581