Consequences on ethylene metabolism of inactivating the ethylene receptor sites in diseased non-climacteric fruit

Abstract

Penicillium digitatum -infected grapefruit synthesize large quantities of the stress hormone ethylene. The compound 1-methylcyclopropene (1-MCP) inhibits the binding of ethylene to the ethylene receptor site, the ethylene binding protein (EBP). Treating infected fruit with 1-MCP prevented infection-induced degreening, such that fumigated fruit retained their green immature color compared to yellow non-fumigated controls. However, 1-MCP treatment significantly increased whole fruit ethylene production. In flavedo tissue of infected non-1-MCP treated fruit, 1-aminocyclopropane-1-carboxylate (ACC) synthase transcript accumulation, ACC synthase (ACS) enzyme activity, ACC and ethylene synthesis were all significantly higher +5 mm ahead of the lesion front than in uninfected non-1-MCP treated controls, but decreased significantly with increased sampling distance away from the lesion. 1-MCP treatment increased ethylene production in infected fruit at all three sampling distances compared to the non-fumigated samples. Even in the absence of infection, 1-MCP treatment resulted in increased ethylene synthesis. The results suggest that, in the presence of a pathogenic stress, blocking the EBPs prevented regulatory control of the ethylene biosynthetic pathway that resulted in an uninhibited expression of the ACS stress-associated genes, increased ACS activity and elevated ACC accumulation and ethylene production. Blocking of the EBPs with 1-MCP did not affect progression of the pathogen through the fruit.