Search

To cause rice blast disease, the fungus Magnaporthe oryzae produces biotrophic invasive hyphae that secrete effectors at the host–pathogen interface. Effectors facilitate disease development, but some (avirulence effectors) also trigger the host''s resistance gene-mediated hypersensitive response and block disease. The number of cloned M. oryzae avirulence effector genes has recently doubled, largely based on resequencing with a Japanese field isolate and association of avirulence activity with presence/absence polymorphisms in novel genes for secreted proteins. Effectors secreted by hyphae in rice cells accumulate in biotrophic interfacial complexes, and this property correlates with their translocation across plasma membrane into the rice cytoplasm. Interestingly, the translocated effectors moved into surrounding uninvaded cells, suggesting that effectors prepare host cells before the fungus enters them. [Copyright &y& Elsevier]

Magnaporthe oryzae is the causal agent of rice blast disease, a devastating problem worldwide. This fungus has caused breakdown of resistance conferred by newly developed commercial cultivars. To address how the rice blast fungus adapts itself to new resistance genes so quickly, we examined chromosomal locations of AVR-Pita, a subtelomeric gene family corresponding to the Pita resistance gene, in various isolates of M. oryzae (including wheat and millet pathogens) and its related species. We found that AVR-Pita (AVR-Pita1 and AVR-Pita2) is highly variable in its genome location, occurring in chromosomes 1, 3, 4, 5, 6, 7, and supernumerary chromosomes, particularly in rice-infecting isolates. When expressed in M. oryzae, most of the AVR-Pita homologs could elicit Pita-mediated resistance, even those from non-rice isolates. AVR-Pita was flanked by a retrotransposon, which presumably contributed to its multiple translocation across the genome. On the other hand, family member AVR-Pita3, which lacks avirulence activity, was stably located on chromosome 7 in a vast majority of isolates. These results suggest that the diversification in genome location of AVR-Pita in the rice isolates is a consequence of recognition by Pita in rice. We propose a model that the multiple translocation of AVR-Pita may be associated with its frequent loss and recovery mediated by its transfer among individuals in asexual populations. This model implies that the high mobility of AVR-Pita is a key mechanism accounting for the rapid adaptation toward Pita. Dynamic adaptation of some fungal plant pathogens may be achieved by deletion and recovery of avirulence genes using a population as a unit of adaptation. [ABSTRACT FROM AUTHOR]

Rice expressing the Pi-ta gene is resistant to strains of the rice blast fungus, Magnaporthe grisea, expressing AVR-Pita in a gene-for-gent relationship. Pi-ta encodes a putative cytoplasmic receptor with a centrally localized nucleotide-binding site and leucine-rich domain (LRD) at the C-terminus. AVR-Pita is predicted to encode a metalloprotease with an N-terminal secretary signal and pro-protein sequences. AVR-Pita176 lacks the secretary and proprotein sequences. We report here that transient expression of AVR-Pita176 inside plant cells results in a Pi-ta-dependent resistance response. AVR-Pita176 protein is shown to bind specifically to the LRD of the Pi-ta protein, both in the yeast two-hybrid system and in an in vitro binding assay. Single amino acid substitutions in the Pi-ta LRD or in the AVR-Pita176 protease motif that result in loss of resistance in the plant also disrupt the physical interaction, both in yeast and in vitro. These data suggest that the AVR-Pita176 protein binds directly to the Pi-ta LRD region inside the plant cell to initiate a Pi-ta-mediated defense response. [ABSTRACT FROM AUTHOR]