Abstract

Postharvest pathogens can penetrate fruit by breaching the cuticle or directly through wounds, and they show disease symptoms only long after infection. During ripening and senescence, the fruit undergo physiological processes accompanied by a decline in antifungal compounds, which allows the pathogen to activate a mechanism of secretion of small effector molecules that modulate host environmental pH. These result in the activation of genes under their optimal pH conditions, enabling the fungus to use a specific group of pathogenicity factors at each particular pH. New research suggests that carbon availability in the environment is a key factor triggering the production and secretion of small pH-modulating molecules: ammonia and organic acids. Ammonia is secreted under limited carbon and gluconic acid under excess carbon. This mini review describes our most recent knowledge of the mechanism of activation of pH-secreted molecules and their contribution to colonization by postharvest pathogens to facilitate the transition from quiescence to necrotrophic lifestyle.

Highlights

  • The resistance of unripe fruit to pathogen infection and colonization after harvest is considered a dynamic process that is modulated during host maturation and ripening

  • The ability of postharvest pathogens to alter pH locally was initially described for Colletotrichum gloeosporioides, and extended to some other pathogens, such as Alternaria alternata, Botrytis cinerea, Penicillium expansum, Penicillium digitatum, Penicillium italicum, Phomopsis mangiferae, Monilinia fructicola, and Fusarium oxysporum (Prusky et al, 2001, 2004; Rollins and Dickman, 2001; Eshel et al, 2002a,b; Manteau et al, 2003; Davidzon et al, 2010; Miyara et al, 2010, 2012)

  • In each case with Colletotrichum spp., increased ammonium accumulation has been related to enhanced pathogenicity (Alkan et al, 2008, 2009; Miyara et al, 2010)

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Summary

INTRODUCTION

The resistance of unripe fruit to pathogen infection and colonization after harvest is considered a dynamic process that is modulated during host maturation and ripening. A pathogen must be able to overcome the host’s defenses and initiate attack under prevailing physiological and environmental conditions During this period, the pathogen must trigger pathogenicity factors that macerate host tissues and release the nutrients required to sustain its development. The pathogen must trigger pathogenicity factors that macerate host tissues and release the nutrients required to sustain its development Since both the host and the pathogen are living entities, the conditions imposed by the host are critical to inducing susceptibility and activating the pathogen quiescent stage. Host Carbon Affect Pathogen Colonization affect fungal pathogenicity and have not been independently studied (Prusky, 1996) In this mini review, we analyze the conditions that modulate the pathogen’s initial stages of colonization by pH modulation of the host

POSTHARVEST PATHOGENS AND pH MODULATION
GENE MODULATION OF FUNGAL PATHOGENICITY FACTORS
MODULATING THE ACTIVATION OF SMALL SECRETED MOLECULES
Findings
Oxalic acid Oxalic acid
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