Redox status‐mediated regulation of gene expression and virulence in the brown rot pathogen Monilinia fructicola

Abstract

The MfCUT1 gene encoding the major cutinase of Monilinia fructicola, a causal agent of blossom blight and fruit rot of stone fruits, is a virulence factor of the pathogen. The pathogen remains quiescent on stage II fruit, which contain high levels of chlorogenic acid, a quinate ester of caffeic acid (CA). A medium shift system was established to show that MfCUT1 expression is down‐regulated by CA, consistent with previous findings in continuous culture, and by the antioxidants glutathione (GSH), N‐acetyl‐l‐cysteine and ascorbic acid. However, MfCUT1 expression is up‐regulated by the superoxide‐generating oxidant menadione and by the GSH synthesis inhibitor buthionine sulphoximine (BSO). The changes in MfCUT1 transcript levels induced by CA or BSO are related to the levels of intracellular GSH and H2O2. In addition, GSH reductase activity was increased by CA. Monilinia fructicola genes encoding enzymes that may contribute to redox homeostasis (GSH reductase and GSH peroxidase) were cloned and their expression was found to be slightly affected following exposure of cultures to CA. The hybrid tea rose cv. Flaming Peace was identified as an alternative host to complement pathogenicity assays of M. fructicola on stone fruits, which are seasonally restricted. Pathogenicity assays on detached peach fruit and rose petals revealed that CA suppresses and H2O2 enhances formation of brown rot lesions. The results indicate that changes in cellular redox status impact MfCUT1 expression and virulence in M. fructicola, and suggest that redox cycling of GSH is related to this regulation.