Oxalic acid production in Sclerotinia sclerotiorum has long been associated with virulence. Research involving UV-induced, genetically undefined mutants that concomitantly lost oxalate accumulation, sclerotial formation, and pathogenicity supported the conclusion that oxalate is an essential pathogenicity determinant of S. sclerotiorum. However, recent investigations showed that genetically defined mutants that lost oxalic acid production but accumulated fumaric acid could cause disease on many plants and substantiated the conclusion that acidic pH, not oxalic acid per se, is the necessary condition for disease development. Critical evaluation of available evidence showed that the UV-induced mutants harbored previously unrecognized confounding genetic defects in saprophytic growth and pH responsiveness, warranting reevaluation of the conclusions about virulence based on the UV-induced mutants. Furthermore, analyses of the evidence suggested a hypothesis for the existence of an unrecognized regulator responsive to acidic pH. Identifying the unknown pH regulator would offer a new avenue for investigating pH sensing/regulation in S. sclerotiorum and novel targets for intervention in disease control strategies.
Keywords: molecular Koch's postulates; oxalic acid; oxaloacetate acetylhydrolase; pH regulation; pH responsiveness.