An ATP-dependent protease homolog ensures basic standards of survival and pathogenicity for Magnaporthe oryzae

Abstract

The occurrence of fungal disease of crops requires a susceptible host, a virulent race, and a favourable environment. Environmental factors play crucial roles and ultimately determine epidemic of disease in host-pathogen interactions. However, the molecular basis of how fungi cope with environments still needs further research. Here, we characterized a lesion-restricted mutant of Magnaporthe oryzae, in which a M agnaporthe ATP-dependent Protease homolog (MAP1) was disrupted by a T-DNA insertion. The gene deletion and complementation transformants (ΔMAP1, ΔMAP1/MAP1) were genetically created and functionally analyzed. Under optimum conditions, no visible phenotypic variations were found in ΔMAP1; but under selected stresses, the significant difference in vegetative growth between ΔMAP1 and wild type (or ΔMAP1/MAP1) emerged, clearly reflecting a causal relationship between MAP1 and stress resistance. The MAP1 protein was subcellularly localized in mitochondria. When subjected to oxidative stress, ΔMAP1 mitochondria were more susceptible to damage than that of the wild type. Linking the decreased virulence in ΔMAP1, we thus propose MAP1, as a protective factor, is required for plant infection and multi-stress resistance. Above all, the MAP1 mutation implies a basic requirement for disease development in the field and a potential implication in crop protection.