Carbon regulation of metabolic processes contributing to pathogenicity by postharvest pathogens

Fruit pathogens can contribute to acidification or alkalization of the fruit host environment. This capability has been used to divide fungal pathogens into acidifying and/or alkalizing classes. Diverse classes of fungal pathogens—Colletotrichum gloeosporioides, Penicillium expansum, Aspergillus nidulans, and Fusarium oxysporum—secrete small pH-affecting molecules. These molecules modify the environmental pH that dictates acidic or alkaline colonizing strategies and induce the expression of PACC-dependent genes. In C. gloeosporioides we have showed that limited or excess of carbon may lead to increase or decrease, respectively, of environmental pH resulting in differential mechanism of fungal pathogenicity. In P. expansum increase in sucrose culture amendment from 15 to 175 mM decreased the accumulation of the mycotoxin patulin suggesting a negative regulation of the global regulator laeA. However functional analysis of CreA, the global carbon catabolite regulator suggested that LaeA and CreA appear to independently regulate secondary metabolism as patulin synthesis as laeA expression was restored in creA deletion in sucrose media, while patulin production was not. Our present results indicate that host sugar changes during fruit ripening in the postharvest life, may modulate environmental pH to enhance fungal pathogenicity by activation of pathogenicity factors and secondary metabolism production.