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The fully recessive disease resistance (R) gene xa13, which mediates race-specific resistance to Xanthomonas oryzae pv. oryzae (Xoo), encodes a plasma membrane protein that differs by one amino acid from that encoded by its dominant (susceptible) allele Xa13. The molecular mechanism of xa13-mediated resistance is largely unknown. Here we show that, compared with its dominant allele, expressional non-reaction of xa13 to Xoo infection, not its protein composition, is the key factor for xa13-mediated resistance. We used the promoter (P(Xa13)) of the dominant Xa13, which was induced by only the incompatible Xoo strain for xa13, to regulate xa13 and xa13(Leu49) (a natural recessive allele of xa13) in the rice line IRBB13 carrying xa13. The transgenic plants showed the same level of susceptibility and bacterial growth rate as those of the rice line carrying dominant Xa13, accompanied by the induced accumulation of xa13 or xa13(Leu49) proteins. Constitutive expression of dominant XA13 or different xa13 proteins (xa13, xa13(Leu49), xa13(Ala85) or xa13(Val184)) in IRBB13 had no effect on Xoo infection in the transgenic plants. These results suggest that race-specific pathogen-induced Xa13 expression is critical for infection. Thus, xa13 stands out from other R genes in that its functions in disease resistance are due to only the loss of pathogen-induced transcriptional motivation caused by natural selection.

Pathogen-Induced Expressional Loss of Function is the Key Factor in Race-Specific Bacterial Resistance Conferred by a Recessive R Gene xa13 in Rice