MoSNF1 regulates sporulation and pathogenicity in the rice blast fungus Magnaporthe oryzae

Yi, Mihwa; Park, Jinhyoung; Ahn, Joong‐Hoon; Lee, Yong-Hwan

doi:10.1016/j.fgb.2008.05.003

Cited by 70 publications

(62 citation statements)

References 56 publications

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“…MoSNF1, a homolog of yeast SNF1, contributes to growth of the colony, shape and germination of the conidia, formation of the appressoria and pathogenicity of the rice blast fungus. 61 rate of appressorium formation between the mutant and wild type. 40 Nevertheless, the mutant is more osmotically sensitive when exposed to 2 M glycerol for 10 min.…”

mentioning

confidence: 96%

Autophagy vitalizes the pathogenicity of pathogenic fungi

Liu

Gao

et al. 2012

Autophagy

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confidence: 96%

Autophagy vitalizes the pathogenicity of pathogenic fungi

Liu

Gao

et al. 2012

Autophagy

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“…Deregulation of AMPK signaling in humans has been linked to type 2 diabetes, heart disease, and cancer (for a review, see reference 16). Snf1 homologs of pathogenic fungi have been implicated in virulence and drug resistance (23,63,64).…”

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confidence: 99%

Roles of the Snf1-Activating Kinases during Nitrogen Limitation and Pseudohyphal Differentiation in Saccharomyces cerevisiae

et al. 2010

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In Saccharomyces cerevisiae, Snf1 protein kinase is important for growth on carbon sources that are less preferred than glucose. When glucose becomes limiting, Snf1 undergoes catalytic activation, which requires phosphorylation of its T-loop threonine (Thr210). Thr210 phosphorylation can be performed by any of three Snf1-activating kinases: Sak1, Tos3, and Elm1. These kinases are redundant in that all three must be eliminated to confer snf1⌬-like growth defects on nonpreferred carbon sources. We previously showed that in addition to glucose signaling, Snf1 also participates in nitrogen signaling and is required for diploid pseudohyphal differentiation, a filamentous-growth response to nitrogen limitation. Here, we addressed the roles of the Snf1-activating kinases in this process. Loss of Sak1 caused a defect in pseudohyphal differentiation, whereas Tos3 and Elm1 were dispensable. Sak1 was also required for increased Thr210 phosphorylation of Snf1 under nitrogen-limiting conditions. Expression of a catalytically hyperactive version of Snf1 restored pseudohyphal differentiation in the sak1⌬/sak1⌬ mutant. Thus, while the Snf1-activating kinases exhibit redundancy for growth on nonpreferred carbon sources, the loss of Sak1 alone produced a significant defect in a nitrogenregulated phenotype, and this defect resulted from deficient Snf1 activation rather than from disruption of another pathway. Our results suggest that Sak1 is involved in nitrogen signaling upstream of Snf1.

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“…Normalization and comparison of mean Ct values were performed as described [79]. To compare relative abundance of transcripts of target genes, the mean threshold cycle (Ct) of triplicate reactions was normalized by that of M. oryzae cyclophilin gene (CYP1, MGG10447), which displayed stable expressions in the developmental stages (unpublished data) and used previously [78,80,81], or by that of O. sativa elongation factor 1a gene (Os03g08020, [82]). Fold changes were compared among treatments or conditions with standard condition.…”

Section: Nucleic Acid Manipulation and Polymerase Chain Reactionmentioning

confidence: 99%

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

2016

Phytopathology in Plants

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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 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.

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MoSNF1 regulates sporulation and pathogenicity in the rice blast fungus Magnaporthe oryzae

Cited by 70 publications

References 56 publications

Autophagy vitalizes the pathogenicity of pathogenic fungi

Autophagy vitalizes the pathogenicity of pathogenic fungi

Roles of the Snf1-Activating Kinases during Nitrogen Limitation and Pseudohyphal Differentiation in Saccharomyces cerevisiae

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

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