NAR-1 AND NAR-2, 2 LOCI REQUIRED FOR MLA(12)-SPECIFIED RACE-SPECIFIC RESISTANCE TO POWDERY MILDEW IN BARLEY

Previously isolated susceptible host mutants were used in a genetic an d functional study of the resistance response of barley specified by r esistance gene Mla(12) to the fungal pathogen Erysiphe graminis f sp h ordei. Mutant M66 represents a defective allele of Mla(12), whereas M2 2, M82, and M100 represent mutations in loci unlinked to Mla(12). Inte rmutant crosses of the latter three show that susceptibility in M82 an d M100 is caused by allelic, recessive mutations that define the Nar l gene (necessary for Mla(12) resistance gene 1), whereas the semidomin ant mutation in M22 defines a second unlinked locus, Nar P. We show th at both genes are required for resistance specified by Mla(12) in diff erent genetic backgrounds of barley. Nar l maps on barley chromosome 2 within an similar to 6-centimorgan restriction fragment length polymo rphism interval: this is 0.5 centimorgans from the anthocyanin pigment ation gene Ant2. Quantitative cytological analysis showed that functio nal alleles of Mla(12), Nar-1, and Nar-2 are required for triggering a cell death reaction of attacked host cells at early stages during inf ection. Functional alleles of all three genes were also required for h igh-level transcript accumulation of barley defense-related genes that encode chitinase, peroxidase, and pathogenesis-related protein-1. The data support the hypothesis that host cell death and high-level accum ulation of defense-related gene transcripts, which are under common co ntrol of Mla(12), Nar-1, and Nar-2, are crucial events of race-specifi c resistance to powdery mildew.