The use of chemical genomics to detect functional systems affecting the non-host disease resistance of pea to Fusarium solani f. sp. phaseoli

Non-host resistance is more durable than race-specific resistance and may involve more signaling systems than race-specific resistance. An array of chemicals capable of specifically inhibiting/affecting most of the vital systems of the plant cell was employed to evaluate a range of systems vital in promoting non-host resistance in the Fusarium solani f. sp. phaseoli/pea endocarp interaction. The parameters measured included pisatin synthesis, hypersensitive discoloration, fungal growth, PR gene induction, and DNA damage. Specific inhibitors of protein phosphatases 1 and 2A (calyculin A, okadaic acid, cantharidin and endothall) and two kinase inhibitors (staurosporine and K-252a from Nocardiopsis sp.) were comparable to fungal challenge in inducing pisatin accumulation. These treatments could often break non-host resistance to a bean pathogen, F. solani f. sp. phaseoli. At low concentrations the treatments transiently enhanced resistance to the pea pathogen, F. solani f. sp. pisi. Nitric oxide and superoxide-generating compounds, salicylic acid, methyl salicylate, and jasmonic acid implicated, as effectors in other systems had no major detectable effect. Thus the broad array of inhibitors delineated cellular functions associated with non-host disease resistance in pea and tentatively excluded some signaling systems reported in other systems.