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Chi, Myoung-Hwan,Park, Sook-Young,Kim, Soonok,Lee, Yong-Hwan Public Library of Science 2009 PLoS pathogens Vol.5 No.4
<▼1><P>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, <I>DES1</I>, in <I>Magnaporthe oryzae</I> regulates counter-defenses against host basal resistance. The <I>DES1</I> 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 <I>DES1</I> 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 cell wall integrity. The <I>Δdes1</I> 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 <I>Δdes1</I> mutant. In the interaction with a susceptible rice cultivar, rice cells inoculated with the <I>Δdes1</I> 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 <I>Δdes1</I> 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 <I>Δdes1</I> mutant. Furthermore, the <I>Δdes1</I> mutant recovered its normal infectious growth in DPI-treated plant tissues. These results suggest that <I>DES1</I> functions as a novel pathogenicity gene that regulates the activity of fungal proteins, compromising ROS-mediated plant defense.</P></▼1><▼2><P><B>Author Summary</B></P><P>Coevolution of plants and microbial pathogens leads to interactions that resemble a molecular war. Pathogens generate effector molecules to infect their hosts, and plants produce defense molecules against pathogen attacks. Interactions between these molecules results in plant immunity or disease. Plant disease could be likened to a complex and delicate matter of balance, where a number of molecules are involved in the battlefield. Discovering and understanding the tipping points in the battle are vital for developing disease-free crops. In the interaction of rice and rice blast fungus, a microbe sensor on rice stimulates the generation of reactive oxygen species (ROS) at the site of infection. ROS is known as an antimicrobial material and a stimulator for defense signaling that is important for preparing reinforcement in neighboring tissues. This paper presents the counter-defense mechanism of the fungus against plant-driven ROS. We found that a pathogenicity factor from rice blast fungus, DES1 (<U>De</U>fense <U>S</U>uppressor 1), is involved in overcoming oxidative stress for the counter-defense mechanism, suggesting that this gene is required for fungal pathogenicity.</P></▼2>