ABSTRACT In two cases, mutations in the same brassinosteroid-related genes caused different phenotypes in japonica varieties Nipponbare and Taichung 65. The mutant phenotypes were less severe in the Taichung 65 background than in the Nipponbare background. Three newly isolated brassinosteroid-insensitive mutants (d61-1N, d61-11, and d61-12) derived from a Nipponbare mutant library werefound to be alleles of d61, which represent defects in the OsBRI1 gene. Although the Nipponbare-derived mutant d61-1N had the same nucleotide substitution as the previously characterized Taichung 65-derived mutant d61-1T, these two mutants showed different phenotypes for plant stature, internode elongation pattern, and seed shape; in each case, d61-1N (in the Nipponbare genetic background) had the more severe mutant phenotype. Similar trends were seen for phenotypes caused by mutants of d2, a brassinosteroid biosynthesis gene. Consistent with these phenotypes, the expression of brassinosteroid-responsive genes was lower in the Nipponbare-derived mutants. These results can be explained by our findings that feed-forward up-regulation of OsBRI1 did not occur in the Nipponbare-derived mutants and that an mPing transposon is inserted into the promoter region of Nipponbare OsBRI1. Based on these results, we conclude that the expression of OsBRI1, especially its feed-forward up-regulation, is misregulated in wild-type Nipponbare and in brassinosteroid-related mutants in a Nipponbare genetic background. AlthoughNipponbare is a model rice genotype, it can be categorized as an OsBRI1 mutant that has reduced sensitivity to brassinosteroid.
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