We characterized five lesion-mimic mutants of rice (
Oryza sativa L.),
spotted leaf 5-2 (
spl5-2),
Spl12,
spl13,
spl14 and
Spl15, all of which have broad-spectrum resistance to the rice blast fungus
Magnaporthe grisea and the bacterial blight pathogen
Xanthomonas campestris pv.
oryzae. First, we analyzed the influence of gene dosage on disease resistance and lesion-mimicry. Although the frequency of lesion-mimicry was lower in heterozygous
Spl12 plants than in homozygous plants, the heterozygotes had almost the same levels of resistance to rice blast and bacterial blight as the homozygotes. Second, we analyzed whether developmental regulation of disease resistance differed in dominant and recessive mutants. We inoculated leaves at different leaf positions at the heading stage with bacterial blight, and found that
spl5-2 and
Spl12 mutants displayed enhanced resistance in lower and upper leaves but the level of resistance was higher in the upper leaves. Furthermore, we clarified the disease resistance and lesion-mimicry by inoculating the top expanded leaves at various developmental stages with bacterial blight. The dominant mutants (
Spl12 and
Spl15) showed lesion-mimicry from an earlier stage than did the recessive mutants (
spl5-2,
spl13 and
spl14); the lesion-mimicry was more severe, and their resistance was rather greater, than in the recessive mutants. Finally, we studied the phenotypes of the progeny of crosses between the
spl mutants. Although the lesion-mimicry of the
Spl12 spl14 double mutant was additive, the resistance phenotype of the double mutant equaled that of
spl14. These results demonstrate that the mechanism by which
SPL genes activate cell death and defense differs among dominant and recessive mutants.
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