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Insidious fungal infections of postharvest pathogens remain quiescent, as biotrophs, during fruit growth and harvest, but activate their development and transform to necrotrophs, which elicit decay symptoms, during ripening and senescence. Exposure of unripe hosts to pathogens quickly initiates defensive signal-transduction cascades that limit fungal growth and development, but exposure to the same pathogens during ripening and storage activates a substantially different signaling cascade that facilitates fungal colonization. The first step in the activation of quiescent infections may involve the fungal capability to cope with plant defense responses by detoxification and efflux transport of antifungals, or by overcoming the suppression of pathogenicity factors. The second step toward the activation of quiescent infections is actively modulated by the pathogen in response to a host signal(s), and includes alkalization or ammonification of the host tissue, which sensitizes the host and activates the transcription and secretion of fungal-degradative enzymes that promote maceration of the host tissue. Feedback signals involving, for example, nitrogen and sugar further enhance pH changes, synthesis of hydrolytic enzymes and saprophytic development in the macerated tissue. This review describes the coordinated series of mechanisms that regulate the activation of quiescent infections in various fruit/vegetable-pathogen interactions.
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Prusky et al. (2007) studied this question.
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