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MST12 Regulates Infectious Growth But Not Appressorium Formation in the Rice Blast Fungus Magnaporthe grisea

March 2002 , Volume 15 , Number  3
Pages  183 - 192

Gyungsoon Park , 1 Chaoyang Xue , 1 Li Zheng , 2 Stephen Lam , 2 and Jin-Rong Xu 1

1Department of Botany and Plant Pathology, Purdue University, West Lafayette, IN 47907 U.S.A.; 2Syngenta, 3054 Cornwallis Road, Research Triangle Park, NC 27709 U.S.A.

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Accepted 14 November 2001.

In the rice blast fungus Magnaporthe grisea, a mitogen-activated protein kinase gene, PMK1, is known to regulate ap-pressorium formation and infectious hyphae growth. Since PMK1 is homologous to the FUS3 and KSS1 genes that regulate the transcription factor STE12 in yeast, we functionally characterized the STE12 homologue in M. grisea (MST12). A polymerase chain reaction-based approach was used to isolate the MST12 gene that is homologous to yeast STE12. Four mst12 deletion mutants were isolated by gene replacement. No obvious defect in vegetative growth, conidiation, or conidia germination was observed in mst12 mutants. However, mst12 mutants were nonpathogenic on rice and barley leaves. In contrast to pmk1 mutants that did not form appressoria, mst12 mutants produced typical dome-shaped and melanized appressoria. However, the ap-pressoria formed by mst12 mutants failed to penetrate onion epidermal cells. When inoculated through wound sites, mst12 mutants failed to cause spreading lesions and appeared to be defective in infectious growth. These data indicate that MST12 may function downstream of PMK1 to regulate genes involved in infectious hyphae growth. A transcription factor or factors other than MST12 must exist in M. grisea and function downstream from PMK1 for ap-pressorium formation.

Additional keyword: fungal pathogenicity .

© 2002 The American Phytopathological Society