Limits...
A novel pathogenicity gene is required in the rice blast fungus to suppress the basal defenses of the host.

Chi MH, Park SY, Kim S, Lee YH - PLoS Pathog. (2009)

Bottom Line: For successful colonization and further reproduction in host plants, pathogens need to overcome the innate defenses of the plant.Targeted gene deletion of DES1 had no apparent effect on developmental morphogenesis, including vegetative growth, conidial germination, appressorium formation, and appressorium-mediated penetration.These results suggest that DES1 functions as a novel pathogenicity gene that regulates the activity of fungal proteins, compromising ROS-mediated plant defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Agricultural Biotechnology, Center for Fungal Genetic Resources, and Center for Fungal Pathogenesis, Seoul National University, Seoul, Korea.

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 Deltades1 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 Deltades1 mutant. In the interaction with a susceptible rice cultivar, rice cells inoculated with the Deltades1 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 Deltades1 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 Deltades1 mutant. Furthermore, the Deltades1 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.

Show MeSH

Related in: MedlinePlus

The Magnaporthe oryzae T-DNA mutant ATMT0144A2 has defects in lesion development and conidial morphology.(A) Rice seedlings (Nakdongbyeo) were inoculated with the wild-type strain 70-15 (left) and ATMT0144A2 (right). Diseased leaves were harvested 7 days after spray inoculation with conidial suspension (1×105 conidia/ml). (B) Light microscopy of conidia produced by 70-15 (top) and ATMT0144A2 (bottom). Bar = 20 µm. (C) Conidial size of the wild type and ATMT0144A2. Values are the mean±SD from >100 conidia of each strain, which were measured using the Axiovision image analyzer. Length is the distance from the base to apex of conidia. Width is the size of the longest septum.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2668191&req=5

ppat-1000401-g001: The Magnaporthe oryzae T-DNA mutant ATMT0144A2 has defects in lesion development and conidial morphology.(A) Rice seedlings (Nakdongbyeo) were inoculated with the wild-type strain 70-15 (left) and ATMT0144A2 (right). Diseased leaves were harvested 7 days after spray inoculation with conidial suspension (1×105 conidia/ml). (B) Light microscopy of conidia produced by 70-15 (top) and ATMT0144A2 (bottom). Bar = 20 µm. (C) Conidial size of the wild type and ATMT0144A2. Values are the mean±SD from >100 conidia of each strain, which were measured using the Axiovision image analyzer. Length is the distance from the base to apex of conidia. Width is the size of the longest septum.

Mentions: A T-DNA insertion mutant (ATMT0144A2) showing reduced virulence was identified from the M. oryzae ATMT mutant library [26]. This mutant developed restricted resistant-type lesions on a susceptible rice cultivar, Nakdongbyeo, and the number of lesions was much less than in the wild-type strain 70-15 (Fig. 1A). In addition, the mutant produced broader ellipsoidal conidia that were uniform and easily detected under a microscope (Fig. 1B). The conidia of the mutant were on average ∼4 µm shorter and ∼3 µm wider than those of the wild type (Fig. 1C). The T-DNA insertion mutant was not significantly defective in any other mycological phenotype tested, although the mycelial growth rate of ATMT0144A2 was slightly faster than that of the wild type on agar medium (Table 1); the colony morphology of the mutant, however, was indistinguishable from that of the wild type (Fig. S1A). Despite the alteration in conidial morphology, conidia produced by the mutant had no defects in conidial adhesion, germination, and appressorium formation (Table 1). These phenotypes imply that the T-DNA insertion in ATMT0144A2 affects pathogenicity and conidial morphogenesis, but not other pre-penetration developmental stages.


A novel pathogenicity gene is required in the rice blast fungus to suppress the basal defenses of the host.

Chi MH, Park SY, Kim S, Lee YH - PLoS Pathog. (2009)

The Magnaporthe oryzae T-DNA mutant ATMT0144A2 has defects in lesion development and conidial morphology.(A) Rice seedlings (Nakdongbyeo) were inoculated with the wild-type strain 70-15 (left) and ATMT0144A2 (right). Diseased leaves were harvested 7 days after spray inoculation with conidial suspension (1×105 conidia/ml). (B) Light microscopy of conidia produced by 70-15 (top) and ATMT0144A2 (bottom). Bar = 20 µm. (C) Conidial size of the wild type and ATMT0144A2. Values are the mean±SD from >100 conidia of each strain, which were measured using the Axiovision image analyzer. Length is the distance from the base to apex of conidia. Width is the size of the longest septum.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2668191&req=5

ppat-1000401-g001: The Magnaporthe oryzae T-DNA mutant ATMT0144A2 has defects in lesion development and conidial morphology.(A) Rice seedlings (Nakdongbyeo) were inoculated with the wild-type strain 70-15 (left) and ATMT0144A2 (right). Diseased leaves were harvested 7 days after spray inoculation with conidial suspension (1×105 conidia/ml). (B) Light microscopy of conidia produced by 70-15 (top) and ATMT0144A2 (bottom). Bar = 20 µm. (C) Conidial size of the wild type and ATMT0144A2. Values are the mean±SD from >100 conidia of each strain, which were measured using the Axiovision image analyzer. Length is the distance from the base to apex of conidia. Width is the size of the longest septum.
Mentions: A T-DNA insertion mutant (ATMT0144A2) showing reduced virulence was identified from the M. oryzae ATMT mutant library [26]. This mutant developed restricted resistant-type lesions on a susceptible rice cultivar, Nakdongbyeo, and the number of lesions was much less than in the wild-type strain 70-15 (Fig. 1A). In addition, the mutant produced broader ellipsoidal conidia that were uniform and easily detected under a microscope (Fig. 1B). The conidia of the mutant were on average ∼4 µm shorter and ∼3 µm wider than those of the wild type (Fig. 1C). The T-DNA insertion mutant was not significantly defective in any other mycological phenotype tested, although the mycelial growth rate of ATMT0144A2 was slightly faster than that of the wild type on agar medium (Table 1); the colony morphology of the mutant, however, was indistinguishable from that of the wild type (Fig. S1A). Despite the alteration in conidial morphology, conidia produced by the mutant had no defects in conidial adhesion, germination, and appressorium formation (Table 1). These phenotypes imply that the T-DNA insertion in ATMT0144A2 affects pathogenicity and conidial morphogenesis, but not other pre-penetration developmental stages.

Bottom Line: For successful colonization and further reproduction in host plants, pathogens need to overcome the innate defenses of the plant.Targeted gene deletion of DES1 had no apparent effect on developmental morphogenesis, including vegetative growth, conidial germination, appressorium formation, and appressorium-mediated penetration.These results suggest that DES1 functions as a novel pathogenicity gene that regulates the activity of fungal proteins, compromising ROS-mediated plant defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Agricultural Biotechnology, Center for Fungal Genetic Resources, and Center for Fungal Pathogenesis, Seoul National University, Seoul, Korea.

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 Deltades1 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 Deltades1 mutant. In the interaction with a susceptible rice cultivar, rice cells inoculated with the Deltades1 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 Deltades1 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 Deltades1 mutant. Furthermore, the Deltades1 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.

Show MeSH
Related in: MedlinePlus