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CPMK2, an SLT2‐homologous mitogen‐activated protein (MAP) kinase, is essential for pathogenesis of Claviceps purpurea on rye: evidence for a second conserved pathogenesis‐related MAP kinase cascade in phytopathogenic fungi
Author(s) -
Mey Géraldine,
Held Katrin,
Scheffer Jan,
Tenberge Klaus B.,
Tudzynski Paul
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.03133.x
Subject(s) - biology , appressorium , magnaporthe grisea , mutant , conidiation , gene , virulence , genetics , phenotype , microbiology and biotechnology , neurospora crassa , kinase , protein kinase a , map kinase kinase kinase , crassa , oryza sativa
Summary Cpmk2, encoding a mitogen‐activated protein (MAP) kinasefromtheascomyceteClavicepspurpurea, is an orthologue ofSLT2fromSaccharomyces cerevisiae, the first isolated from a biotrophic, non‐appressorium‐forming pathogen. Deletion mutants obtained by a gene replacement approach show impaired vegetative properties (no conidiation) and a significantly reduced virulence, although they retain a limited ability to colonize the host tissue. Increased sensitivity to protoplasting enzymes indicates that the cell wall structure of the mutants may be altered. As the phenotypes of these mutants are similar to those observed in strains of the rice pathogen,Magnaporthe grisea, that have been deprived of their MAP kinase genemps1, the ability ofcpmk2to complement the defects of Δmps1was investigated. Interestingly, theC. purpureagene, under the control of its own promoter, was able to complement theM. griseamutant phenotype: transformants were able to sporulate and form infection hyphae on onion epidermis and were fully pathogenic on barley leaves. This indicates that, despite the differences in infection strategies, which include host and organ specificity, mode of penetration and colonization of host tissue, CPMK2/ MPS1 defines a second MAP kinase cascade (after the Fus3p/PMK1 cascade) essential for fungal pathogenicity.