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ARS Home » Research » Publications at this Location » Publication #125522


item McEvoy, James
item Saftner, Robert
item Conway, William
item Jones, Richard

Submitted to: Biochemistry and Cell Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/7/2003
Publication Date: 1/1/2004
Citation: Prusky, D., Mcevoy, J.L., Saftner, R.A., Conway, W.S., Jones, R.W. 2003. Relationship between host acidification and virulence of penicillium spp. on apple and citrus fruit. Biochemistry and Cell Biology. Phytopathology Vol. 94, No. 1, 2004, page 44-51

Interpretive Summary: Substantial losses of apple fruit in storage can be caused by postharvest pathogens. Although many of these diseases can be controlled by fungicides, consumer's concerns about the association of these chemicals with human maladies may limit their future application. To reduce storage losses, alternate methods of postharvest disease control must be found. Postharvest pathogens can produce polygalacturonase, a cell wall degrading enzyme, to invade fruit leading to decay. We found that oxalic acid accumulation can affect pathogenicity. Oxalic acid accumulation results in a decrease in fruit pH at the infection site, leading to an increase in polygalacturonase production and greater decay. This discovery may be used by plant breeders looking for ways to retard oxalic acid accumulation by fungi and reduce decay. Fruit packing and storage facilities may then be able to reduce the amount of fungicides used to maintain fruit quality in storage.

Technical Abstract: Penicillium expansum, P.digitatum, and P. italicum acidify the ambient environments of apple and citrus fruit during decay development. They use two mechanisms for this: the production of organic acids, mainly citric and gluconic, and NH4+ utilization associated with H+ efflux. Exposure of P. expansum and P. digitatum hyphae to pH 5.0 increased their citric acid production, compared with the production of organic acids at acidic ambient pH. In decayed fruit, both pathogens produced significant amounts of citric and gluconic acids in the dacayed tissue and reduced the host pH by 0.5 to 1.0 units. Ammonium depletion from the growth medium or from the fruit tissue was directly related to ambient pH reduction. Analysis of transcripts encoding the endopolygalacturonase gene, pepg1, from P. expansum accumulated under acidic culture conditions from pH 3.5 to 5.0, suggesting that the acidification process is a pathogenicity enhancing factor of Penicillium spp. This hypothesis was supported by the finding that cultivars with lower pH and citric acid treatments to reduce tissue pH increased P. expansum development, presumably by increasing local pH. However, organic acid treatment could not enhance decay development in naturally acidic apples. Conversely, local alkalinization with NaHCO3 reduced decay development. The present results further suggest that ambient pH is a regulatory cue for processes linked to pathogenicity of postharvest pathogens, and that specific genes are expressed as a result of the modified host pH created by the pathogens.