RAR1, ROR1, and the actin cytoskeleton contribute to basal resistance to Magnaporthe grisea in barley.
The fungus Magnaporthe grisea, the causal agent of rice blast disease, is a major pathogen of rice and is capable of producing epidemics on other cultivated cereals, including barley (Hordeum vulgare). We explored the requirements for basal resistance of barley against a compatible M. grisea isolate using both genetic and chemical approaches. Mutants of the RAR1 gene required for the function of major resistance gene-mediated resistance and mutants of the ROR1 and ROR2 genes required for full expression of cell-wall-penetration resistance against powdery mildew pathogens were examined for macroscopic and microscopic alterations in M. grisea growth and symptoms. RAR1 contributed to resistance in epidermis and mesophyll at different stages of fungal infection dependent on the MLO/mlo-5 status. Whereas no ROR2 effect was detected, ROR1 was found to contribute to cell-wall-penetration resistance, at least in the epidermis. Application of the actin agonist cytochalasin E promoted cell wall penetration by M. grisea in a dose-dependent manner, demonstrating an involvement of the actin cytoskeleton in penetration resistance.[1]References
- RAR1, ROR1, and the actin cytoskeleton contribute to basal resistance to Magnaporthe grisea in barley. Jarosch, B., Collins, N.C., Zellerhoff, N., Schaffrath, U. Mol. Plant Microbe Interact. (2005) [Pubmed]
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