Abstract
As biotrophs, insidious fungal infections of postharvest pathogens remain quiescent during fruit growth while at a particular phase during fruit ripening and senescence the pathogens transform to necrotrophs causing typical decay symptoms. Exposure of unripe hosts to pathogens (hemi-biotroph or necrotrophs), initiates defensive signal-transduction cascades that limit fungal growth and development. Exposure to the same pathogens during ripening and storage activates a substantially different signalling cascade which facilitates fungal colonization. This chapter will focus on modulation of postharvest host-pathogen interactions by pH and the consequences of these changes. Host pH can be raised or lowered in response to host signals, including alkalization by ammonification of the host tissue as observed in Colletotrichum and Alternaria, or acidification by secretion of organic acids as observed in Penicillium, Botrytis and Sclerotinia. These changes sensitize the host and activate transcription and secretion of fungal hydrolases that promote maceration of the host tissue. Several particular examples of coordinated responses which follow this scheme are described.
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