Testing a two phase model of broad-host range necrotrophic compatibility

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This project is broadly focused on understanding the fundamental mechanisms by which aggressive, broad host range plant pathogens are able to cause disease on diverse groups of plants. The specific focus is on the fungal plant pathogen Sclerotinia sclerotiorum, the cause of white mold disease in soybean, sunflower, cole crops, pulse crops and a variety of others. In total, this agricultural pathogen infects over 600 plant species and accounts for an estimated $200 million in annual economic loss in the U.S. Market losses can be extremely high when disease outbreaks occur on a large scale; the U.S. soybean stem rot outbreak in 2009, for instance, directly reduced harvests by approximately $560 million. In the field, diseases caused by S. sclerotiorum are challenging to control for the lack of resistant cultivars effective against this pathogen and the long survival properties of the fungus. In Florida, losses occurring in crops of green bean, carrot, Brassica carinata, bell pepper and cabbage are of perennial concern. This research addresses the need to elucidate the genetically based mechanisms of S. sclerotiorum that are required for its aggressiveness and the genetic factors from the host that account for susceptibility or resistance to the pathogen. This information is fundamentally important for the long-term purpose of developing effective disease control strategies against this devastating fungal pathogen. This research will have the broader impact of training undergraduates recruited from the University of Florida Undergraduate Research Minority Participation Program in molecular genetic techniques using cutting edge tools for genome manipulation. This project aims to elucidate factors that underlie the establishment of basic compatibility in broad host range necrotrophic pathogens. The working model is that these pathogens, exemplified by Sclerotinia sclerotiorum, utilize a two-phase strategy for establishing basic compatibility and host colonization. From this model two hypotheses are possible.The first hypothesis is that basic host-pathogen compatibility across a broad range of hosts is established by pathogen targeting of universally conserved host targets (e.g., MED16). The alternative, but not mutually exclusive, hypothesis is that these pathogens have evolved and utilize independent virulence factors and effectors for different hosts to overcome host-specific defenses (e.g., glucosinolates). One discovery-based and two targeted Specific Objectives will test these hypotheses. The first is to create and phenotype gene-specific loss-of-function mutations for select members of the predicted S. sclerotiorum secretome chosen from transcriptome data. The second objective is to characterize the pathway of Arabidopsis Mediator complex subunit 16 (MED16) protein modification and degradation to understand its role in broad host range necrotrophic pathogen susceptibility and resistance. The final objective is to determine the role of MED16 degradation in host susceptibility to S. sclerotiorum and other broad host range necrotrophic pathogens. Plant disease resistance to this class of pathogens lags behind the understanding of other classes of host-pathogen interactions. The genetically complex nature of these interactions is a major factor limiting understanding. Utilizing new molecular genetic tools and genomic resources, the proposed research will establish greater mechanistic understanding of broad host range necrotrophic pathogen-host compatibility.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.