Regulatory Components for Host Recognition by a Fungal Plant Pathogen
University Of Maryland, College Park, College Park MD
Investigators
Abstract
Plant pathogenic fungi have developed traits that allow their entry and pathogenesis on specific host plants. A key adaptation is the regulation of these traits so that they are expressed at the appropriate time and level, as well as on the correct host. This project focuses upon fungal recognition a host-specific compound for the regulation of its virulence traits. Pisatin, an antimicrobial isoflavonoid, is produced specifically by garden pea (Pisum sativum) as a phytoalexin. Nectria haematococca (anamorph Fusarium solani), a pathogen of pea, is able to recognize and respond to the presence of this host compound. One pisatin-induced trait is the expression of the pisatin demethylase gene (PDA1), which encodes a cytochrome P450 that detoxifies pisatin. Other traits involved in pea pathogenicity are also induced by pisatin, suggesting that pisatin acts as a host-selective cue to coordinate expression of these different traits. Previous NSF-supported research identified a 40 bp regulatory element on the PDA1 promoter that provides the pisatin-response. Manipulation of regulatory elements in the promoter showed that pisatin is the major signal controlling PDA1 expression during pea pathogenesis. A gene encoding a DNA-binding protein that specifically binds the 40 bp pisatin-responsive element was identified using the yeast one-hybrid system. The goal of this project is to test if the encoded DNA-binding protein is a direct determinant of pisatin-responsive PDA1 expression. Transformation will be used to perform targeted gene disruption of this gene in N. haematococca. The effect of disruption upon the pisatin-inducibility PDA1 will be determined. A loss of pisatin-responsive expression will be significant in indicating direct function in pisatin signaling. This will allow future experiments to test if the same DNA-binding protein controls other pisatin-induced pea pathogenicity traits as well. Overall, these results will provide a model of a signaling pathway through which this soilborne plant pathogen is able to chemically detect its host and trigger the traits needed for pathogenesis of that host. This is important for not only understanding the components needed for host-adaptation in plant pathogenesis but for developing future controls of plant disease.
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