- Enhanced Disease Susceptibility 1 and Salicylic Acid Act Redundantly to Regulate Resistance Gene-Mediated Signaling

Abstract

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 cell 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.

A fungal monooxygenase-derived jasmonate attenuates host innate immunity

“…However, unlike in des1Δ and sir2Δ, treatment with the exogenous antioxidants GSH or DPI does not suppress abmΔ-induced accumulation of inclusions in rice plants. Furthermore, though the des1Δ mutant is hypersensitive to exogenous oxidative stress 33 , the abmΔ did not show any sensitivity toward hydrogen peroxide during mycelial growth. In contrast, loss of the M. oryzae glutathione peroxidase Hyr1, whose function is to break down ROS in planta 36 , does not induce deposition of granules or inclusions during host invasion.…”

“…Thus, fungal Abm activity most likely prevents the basal host defense response by keeping phytoalexin levels in check during establishment of the blast fungus. A number of M. oryzae mutants that are impaired in suppressing the basal defense response in rice [33][34][35] , such as des1Δ, sir2Δ and snx41Δ, show increased accumulation of granular deposits, which resemble the inclusions triggered by abmΔ in the invaded rice cells. However, unlike in des1Δ and sir2Δ, treatment with the exogenous antioxidants GSH or DPI does not suppress abmΔ-induced accumulation of inclusions in rice plants.…”

The histone acetyltransferase PsGcn5 mediates oxidative stress responses and is required for full virulence of Phytophthora sojae

“…With respect to the toxicity of ROS molecules and their importance in plant defense responses, plant pathogens have to develop strategies to scavenge ROS for survival in harsh environments and successfully invade host cells [47]. In fungal plant pathogens, several genes have proven to be responsible for ROS detoxification at the infection site, and the defects of these corresponding genes have shown attenuated virulence on host plants [25,27]. In this study, we found that the PsGcn5-silenced mutant had no apparent defects in hyphae growth and cyst germination, but had limited infectious hyphae growth and reduced virulence in the susceptible soybean cv.…”

“…During the interactions between plants and pathogens, scavenging of host-derived ROS at the site of infection is a key mechanism for pathogens to overcome plant defenses and colonise the host [25,27]. We hypothesized that the blocked hyphal growth in the infected cell and reduced virulence of the PsGcn5-silenced mutant were due to a defect in the scavenging of ROS.…”

“…In Claviceps purpurea, deletion of transcriptional factor CPTF1 increases H 2 O 2 accumulation at the invasion site following the defense reaction to pathogen attack [26]. Magnaporthe oryzae gene des1, affecting the expression of related peroxidase and laccase coding genes, is involved in detoxifying ROS at the initial infection site, and des1deletion mutants lose pathogenicity in rice [27]. In M. oryzae, deletion of Moatf1, a homolog of basic leucine zipper (bZIP) transcription factor ATF/CREB in S. pombe regulating the oxidative stress response, caused retarded vegetative growth of mycelia and exhibited higher sensitivity to H 2 O 2 , thereby leading to significantly reduced virulence in rice cv.…”