Fruit pathogens can either acidify or alkalinize the pH of the colonized host environment.This capability has been used to divide fungal pathogens into acidifying and alkalizing classes.We show that diverse classes of fungal pathogens,including;Colletotrichum gloeosporioides,Penicillium expansum,Aspergillus nidulans,Sclerotinia sclerotiorum,and Fusarium oxysporum-secrete small pH-effector molecules.These molecules modify the environmental pH that dictates acidic or alkaline colonization life patterns and select for the activity of PACC-dependent genes.We show that the secretion of pH-effector molecules that contribute to fruit pathogenicity is carbon-dependent.In multiple cross-class organisms,acidification is induced under excess,e.g.175 mM sucrose.This carbon source is metabolized by glucose oxidase(gox2)to gluconic acid,contributing to medium acidification.In contrast,alkalization occurs under conditions of carbon deprivation,e.g.,less than 15 mM sucrose,where catalyzed deamination of non-preferred carbon sources,such as the amino acid glutamate,by glutamate dehydrogenase 2(gdh2)results in the secretion of ammonia.Functional △gdh2 mutants show reduced alkalization and pathogenicity during growth under carbon deprivation,but not in high-carbon media or on fruit rich in sugar,whereas analysis of △gox2 mutants show reduced acidification and pathogenicity in carbon-excess conditions.These insights can reveal that mechanism(s)of fungal pathogenicity in ripening fruits are dependent on the carbon availability of the host that induces differential pH responsiveness during colonization.This indicates that differential pH modulation by fungal pathogens is a universal host-dependent mechanism that modulates environmental pH as a tool to enhance host fruit colonization.