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A Novel Pathogenicity Gene Is Required in the Rice Blast
Fungus to Suppress the Basal Defenses of the Host
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 Authours
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Myoung-Hwan Chi, Sook-Young Park, Soonok Kim, Yong-Hwan Lee |
| Title |
A Novel Pathogenicity Gene Is Required in the Rice Blast
Fungus to Suppress the Basal Defenses of the Host |
| Journal |
PLOS PATHOG, 2009 (5) ~ |
Abstract
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For successful colonization and further reproduction in host plants, pathogens need to overcome the innate defenses of the plant. We demonstrate that a novel pathogenicity gene, DES1, in Magnaporthe oryzae regulates counter-defenses against host basal resistance. The DES1 gene was identified by screening for pathogenicity-defective mutants in a T-DNA insertional mutant library. Bioinformatic analysis revealed that this gene encodes a serine-rich protein that has unknown biochemical properties, and its homologs are strictly conserved in filamentous Ascomycetes. Targeted gene deletion of DES1 had no apparent effect on developmental morphogenesis, including vegetative growth, conidial germination, appressorium formation, and appressorium-mediated penetration. Conidial size of the mutant became smaller than that of the wild type,but the mutant displayed no defects on ce ll wall integrity. The Ddes1 mutant was hypersensitive to exogenous oxidative stress and the activity and transcription level of extracellular enzymes including peroxidases and laccases were severely decreased in the mutant. In addition, ferrous ion leakage was observed in the Ddes1 mutant. In the interaction with a susceptible rice cultivar, rice cells inoculated with the Ddes1 mutant exhibited strong defense responses accompanied by brown granules in primary infected cells, the accumulation of reactive oxygen species (ROS), the generation of
autofluorescent materials, and PR gene induction in neighboring tissues. The Ddes1 mutant displayed a significant reduction in infectious hyphal extension, which caused a decrease in pathogenicity. Notably, the suppression of ROS generation by treatment with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidases, resulted in a significant
reduction in the defense responses in plant tissues challenged with the Ddes1 mutant. Furthermore, the Ddes1 mutant recovered its normal infectious growth in DPI-treated plant tissues. These results suggest that DES1 functions as a novel pathogenicity gene that regulates the activity of fungal proteins, compromising ROS-mediated plant defense. |
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