Host Ammonification by Postharvest Pathogens and its Contribution to Fungal Colonization and Symptom Development

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. A key response to the physiological changes occurring during fruit ripening 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 Colletotrichum sp.), are significantly expressed only under alkaline conditions. In this proposal, investigated the mechanisms by which ammonification and alkalinization of infected tissues by the pathogen affect the host’s defense response to fungal attack, and instead increase compatibility during postharvest pathogen-host interactions. Our hypotheses were:1) that host signals, including ripening-related changes, 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 enhanced fungal colonization, by “suppression of host responses”, including production of reactive oxygen species, activation of superoxide, and polyphenol oxidase production. Our objectives were: 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) analyze hostgene expression in alkalinized regions of fruits attacked by hemibiotrophic fungi.