MAP KINASE AND CAMP SIGNALING REGULATE INFECTION STRUCTURE FORMATION AND PATHOGENIC GROWTH IN THE RICE BLAST FUNGUS MAGNAPORTHE-GRISEA

Many fungal pathogens invade plants using specialized infection struct ures called appressoria that differentiate from the tips of fungal hyp hae contacting the plant surface. We demonstrate a role for a MAP kina se that is essential for appressorium formation and infectious growth in Magnaporthe grisea, the fungal pathogen responsible for rice blast disease. The PMK1 gene of M. grisea is homologous to the Saccharomyces cerevisiae MAP kinases FUS3/KSS1, and a GST-Pmk1 fusion protein has k inase activity in vitro. pmk1 mutants of M. grisea fail to form appres soria and fail to grow invasively in rice plants. pmk1 mutants are sti ll responsive to cAMP for early stages of appressorium formation, whic h suggests Pmk1 acts downstream of a cAMP signal for infection structu re formation. PMK1 is nonessential for vegetative growth and sexual an d asexual reproduction in culture. Surprisingly, when expressed behind the GAL1 promoter in yeast, PMK1 can rescue the mating defect in a fu s3 kss1 double mutant. These results demonstrate that PMK1 is part of a highly conserved MAP kinase signal transduction pathway that acts co operatively with a cAMP signaling pathway for fungal pathogenesis.