Host resistance and pathogen-derived hormone affect the outcome of a fungal-plant interaction

Like most organisms plants must be able to defend themselves from a variety of pathogens throughout their lifetime. In order to achieve this, plants uses a combination of hormone signaling and defense-related gene responses. However, pathogens also have mechanisms to overcome or manipulate these defense strategies in order to inhabit plant hosts. Fusarium oxysporum is a saprophytic filamentous fungus that infects a wide variety of plants and is the causal agent of Fusarium wilt disease. F. oxysporum like other soil borne fungi enters through plant roots where it eventually colonizes the xylem ultimately blocking water and nutrients causing wilt symptoms. Previously, six RESISTANCE TO FUSARIUM OXYSPORUM (RFO) loci were identified in Arabidopsis thaliana Columbia 0 (Col0) accession against F. oxysporum forma specialis matthiolae (garden stock pathogen). RFO1 and RFO2 were identified as a wall-associated kinase-like kinase and receptor-like protein, respectively. Here we discuss the cloning and characterization of another resistance gene, RFO3, in Arabidopsis. RFO3, like RFO1, is a receptor-like kinase (RLK) but belongs to the S Domain 1 (SD1) family. Other members of the SD1 family of RLKs have been shown to be induced by the bacterial pathogen, Xanthamonas campestris. Several pathogens make plant hormones as secondary metabolites. These pathogen-derived hormones can alter plant hormone signaling to make plants more conducive to infection. In plants, jasmonic acid (JA) is considered important for developmental signaling and defense against necrotrophic and insect pathogens. However, we found several strains of F. oxysporum produce significant quantities of JA along with JA conjugated to leucine (JA-Leu) and isoluecine (JA-Ile), which is involved in JA signaling in plants. Furthermore, the JA-Ile/Leu produced by F. oxysporum is biologically relevant because it can activate the JA-responsive gene THI2.1 in Arabidopsis seedlings. Interestingly, Arabidopsis coi1-1 mutants are more resistant to several strains of F. oxypsorum. Also, a higher concentration of F. oxysporum was detected in COI1 wild-type roots compared to coi1 mutant roots. Therefore, F. oxysporum derived JA may interfere with JA signaling through COI1 and is important for making Arabidopsis more susceptibile to F. oxysporum