MST12 regulates infectious growth but not appressorium formation in the rice blast fungus Magnaporthe grisea

Area of Science:

• Plant Pathology
• Molecular Mycology
• Fungal Genetics

Background:

• The rice blast fungus Magnaporthe grisea relies on specific genes for infection.
• Mitogen-activated protein kinase PMK1 is essential for appressorium formation and invasive growth.
• PMK1's yeast homologues, FUS3 and KSS1, regulate the transcription factor STE12.

Purpose of the Study:

• To functionally characterize the STE12 homologue, MST12, in Magnaporthe grisea.
• To determine the role of MST12 in the pathogenicity of M. grisea.
• To elucidate the relationship between PMK1 and MST12 in the fungal infection process.

Main Methods:

• Isolation of the MST12 gene using a polymerase chain reaction-based approach.
• Generation of mst12 deletion mutants via gene replacement.
• Phenotypic analysis of mutants including vegetative growth, conidiation, germination, pathogenicity assays, and appressorial penetration tests.

Main Results:

• MST12 deletion mutants exhibited no defects in vegetative growth, conidiation, or conidia germination.
• mst12 mutants were nonpathogenic on rice and barley, failing to cause spreading lesions.
• While mst12 mutants formed appressoria, they were unable to penetrate host cells, indicating a defect in infectious growth downstream of PMK1.

Conclusions:

• MST12 functions downstream of PMK1, regulating genes essential for infectious hyphae growth in M. grisea.
• MST12 is critical for the invasive stage of fungal infection, but not for appressorium formation itself.
• Other transcription factors likely mediate PMK1's role in appressorium development in M. grisea.