Analysis of the Structure of the <i>AVR1-CO39</i> Avirulence Locus in Virulent Rice-Infecting Isolates of <i>Magnaporthe grisea</i>

Farman, Mark L.; Eto, Yukiko; Nakao, Tomomi; Tosa, Yukio; Nakayashiki, Hitoshi; Mayama, Shigeyuki; Leong, Sally A.

doi:10.1094/mpmi.2002.15.1.6

Cited by 127 publications

(94 citation statements)

References 31 publications

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“…In addition to Slp1, more than a dozen effector proteins have been identified in M. oryzae, such as Pwl2 (for pathogenicity toward weeping lovegrass protein2) (Sweigard et al, 1995), AVR-Pita1 (Jia et al, 2000), AVR-Pia (Miki et al, 2009;Yoshida et al, 2009), AVR-Pik/km/kp, AVR-Pii (Yoshida et al, 2009), AVR-CO39 (Farman et al, 2002), Bas1 to Bas4 (Mosquera et al, 2009), and AvrPiz-t (Li et al, 2009). N-Glycosylation sites are predicted in some of these effector proteins, including Bas2, Bas4, and AvrPiz-t, suggesting that Alg3 may mediate the N-glycosylation of several effector proteins in M. oryzae during plant infection.…”

Section: Discussionmentioning

confidence: 99%

N-Glycosylation of Effector Proteins by an α-1,3-Mannosyltransferase Is Required for the Rice Blast Fungus to Evade Host Innate Immunity

et al. 2014

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Plant pathogenic fungi deploy secreted effectors to suppress plant immunity responses. These effectors operate either in the apoplast or within host cells, so they are putatively glycosylated, but the posttranslational regulation of their activities has not been explored. In this study, the ASPARAGINE-LINKED GLYCOSYLATION3 (ALG3)-mediated N-glycosylation of the effector, Secreted LysM Protein1 (Slp1), was found to be essential for its activity in the rice blast fungus Magnaporthe oryzae. ALG3 encodes an a-1,3-mannosyltransferase for protein N-glycosylation. Deletion of ALG3 resulted in the arrest of secondary infection hyphae and a significant reduction in virulence. We observed that Dalg3 mutants induced massive production of reactive oxygen species in host cells, in a similar manner to Dslp1 mutants, which is a key factor responsible for arresting infection hyphae of the mutants. Slp1 sequesters chitin oligosaccharides to avoid their recognition by the rice (Oryza sativa) chitin elicitor binding protein CEBiP and the induction of innate immune responses, including reactive oxygen species production. We demonstrate that Slp1 has three N-glycosylation sites and that simultaneous Alg3-mediated N-glycosylation of each site is required to maintain protein stability and the chitin binding activity of Slp1, which are essential for its effector function. These results indicate that Alg3-mediated N-glycosylation of Slp1 is required to evade host innate immunity.

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Section: Discussionmentioning

confidence: 99%

N-Glycosylation of Effector Proteins by an α-1,3-Mannosyltransferase Is Required for the Rice Blast Fungus to Evade Host Innate Immunity

et al. 2014

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“…Such gains of virulence are often associated with transposon-mediated inactivation or deletion of PAMP-encoding genes whose products trigger the plant adaptive immune system 37,38 . Thus, an understanding of the natural history of repetitive elements in M. grisea not only provides an insight into their impact on genome evolution but also sheds light on mechanisms of pathogenic variation.…”

Section: Secondary Metabolic Pathways Of M Griseamentioning

confidence: 99%

“…Some rearrangements are expected to have positive fitness benefits, especially those that result in loss of genes whose products would normally trigger defence responses in potential hosts. Many hostspecificity genes in M. grisea are situated in transposon-rich regions of the genome; this arrangement provides ample opportunity for host-range expansion through gene loss 37,41 .…”

Section: Secondary Metabolic Pathways Of M Griseamentioning

confidence: 99%

The genome sequence of the rice blast fungus Magnaporthe grisea

Dean

Talbot

Ebbole

et al. 2005

Nature

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1,502

1,194

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Magnaporthe grisea is the most destructive pathogen of rice worldwide and the principal model organism for elucidating the molecular basis of fungal disease of plants. Here, we report the draft sequence of the M. grisea genome. Analysis of the gene set provides an insight into the adaptations required by a fungus to cause disease. The genome encodes a large and diverse set of secreted proteins, including those defined by unusual carbohydrate-binding domains. This fungus also possesses an expanded family of G-protein-coupled receptors, several new virulence-associated genes and large suites of enzymes involved in secondary metabolism. Consistent with a role in fungal pathogenesis, the expression of several of these genes is upregulated during the early stages of infection-related development. The M. grisea genome has been subject to invasion and proliferation of active transposable elements, reflecting the clonal nature of this fungus imposed by widespread rice cultivation.Outbreaks of rice blast disease are a serious and recurrent problem in all rice-growing regions of the world, and the disease is extremely difficult to control 1,2 . Rice blast, caused by the fungus Magnaporthe grisea, is therefore a significant economic and humanitarian problem. It is estimated that each year enough rice is destroyed by rice blast disease to feed 60 million people 3 . The life cycle of the rice blast fungus is shown in Fig. 1. Infections occur when fungal spores land and attach themselves to leaves using a special adhesive released from the tip of each spore 4 . The germinating spore develops an appressorium-a specialized infection cell-which generates enormous turgor pressure (up to 8 MPa) that ruptures the leaf cuticle, allowing invasion of the underlying leaf tissue 5,6 . Subsequent colonization of the leaf produces disease lesions from which the fungus sporulates and spreads to new plants. When rice blast infects young rice seedlings, whole plants often die, whereas spread of the disease to the stems, nodes or panicle of older plants results in nearly total loss of the rice grain 2 . Different host-limited forms of M. grisea also infect a broad range of grass species including wheat, barley and millet. Recent reports have shown that the fungus has the capacity to infect plant roots 7 .Here we present our preliminary analysis of the draft genome sequence of M. grisea, which has emerged as a model system for understanding plant-microbe interactions because of both its economic significance and genetic tractability 1,2 . Acquisition of the M. grisea genome sequenceThe genome of a rice pathogenic strain of M. grisea, 70-15, was sequenced through a whole-genome shotgun approach. In all, greater than sevenfold sequence coverage was produced, and a summary of the principal genome sequence data is provided in Table 1 and Supplementary Table S1. The draft genome sequence consists of 2,273 sequence contigs longer than 2 kilobases (kb), ordered and orientated within 159 scaffolds. The total length of all sequence contigs is 38.8 mega...

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“…1) Several avirulence factors have been reported from Pyricularia isolates in rice. [2][3][4] Blast fungi might also produce active factors such as host-specific toxins which some fungal pathogens produce as determinants of pathogenicity. 5) Virulence agents produced by Pyricularia isolates have also been examined.…”

mentioning

confidence: 99%

Induction of Chlorosis, ROS Generation and Cell Death by a Toxin Isolated fromPyricularia oryzae

Tsurushima

Minami

Miyagawa

et al. 2010

Bioscience, Biotechnology, and Biochemistry

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Analysis of the Structure of the AVR1-CO39 Avirulence Locus in Virulent Rice-Infecting Isolates of Magnaporthe grisea

Cited by 127 publications

References 31 publications

N-Glycosylation of Effector Proteins by an α-1,3-Mannosyltransferase Is Required for the Rice Blast Fungus to Evade Host Innate Immunity

N-Glycosylation of Effector Proteins by an α-1,3-Mannosyltransferase Is Required for the Rice Blast Fungus to Evade Host Innate Immunity

The genome sequence of the rice blast fungus Magnaporthe grisea

Induction of Chlorosis, ROS Generation and Cell Death by a Toxin Isolated fromPyricularia oryzae

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