Host ammonification by postharvest pathogens and its contribution to fungal colonization and symptom development

Grants and Contracts Details


Postharvest decay of fruits and vegetables caused by pathogenic and saprophytic fungi significantly impairs the quality and quantity of fresh produce brought to market. Consequently, there is considerable interest in identifying factors that determine the susceptibility of these commodities to pathogen infection. Insidious postharvest decays remain quiescent during fruit growth and harvest, but activate during the postharvest period. While unripe, fruit and vegetable hosts exposed to pathogens quickly initiate a defensive signal transduction cascade that limits fungal growth and development. However, during the ripening and storage period exposure of the same hosts to the same pathogens activates a substantially different signaling cascade that facilitates rather than prevents fungal colonization. This transformation from the resistant to the susceptible state involves significant physiological changes that occur naturally in the host, and which are sensed and responded to by the pathogen. A key response to these physiological changes is the initiation of ammonium secretion by the pathogen. Ammonium ions at the infection site (ammonification) have subsequent effects on both the pathogen and the host. An accompanying alkalinization process resulting from ammonia accumulation contributes to pathogenicity, since some important fungal virulence factors, (such as pectate lyase in Col/etotrichum sp, and endo 1,4-~ endoglucanase in Alternaria alternata), are significantly expressed only under alkaline conditions. In this proposal, we want to investigate the mechanisms by which ammonification and alkalinization of infected tissues by the pathogen neutralize the host's defense response to fungal attack, and instead increase compatibility during postharvest pathogen-host interactions. Our hypotheses are: 1) that host signals, including ripening-related changes in pH, induce secretion of ammonia by the pathogen; 2) that ammonia accumulation, and the resultant environmental alkalinization regulate the expression of fungal virulence genes that are essential for postharvest rot development; 3) that ammonification suppresses host responses, including production of reactive oxygen species, activation of superoxide, and polyphenol oxidase production. To test these hypotheses, we will focus on the postharvest infection of tomato fruits by the hemibiotrophic fungus Col/etotrichum coccodes. Our objectives are: to analyze: 1) factor(s) which activate the production and secretion of ammonia by the fungus; 2) fungal gene(s) that play role(s) in the ammonification process; 3) the relationship between ammonification and the activation of host defense response(s) during pathogen colonization; and 4) gene expression in alkalinized regions of fruits attacked by hemibiotrophic fungi.
Effective start/end date12/31/0612/31/10


  • Binational Agricultural Research & Development Fun: $103,000.00


Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.