Since the 1990s, the development of tagging methods has facilitated the isolation and identification of causative genes through the acquisition of loss-of-function mutants. However, a limitation of this approach was its inability to isolate genes with redundant functions. Therefore, I focused on gain-of-function mutants. In this study, numerous rice mutants were generated through activation tagging and Full-length cDNA OvereXpression (FOX), and the causal genes were subsequently isolated and characterized. The Spl18 mutant, which exhibits a lesion-mimic phenotype in the activation tagging lines, was found to result from the overexpression of an uncharacterized acyltransferase gene, OsAT1. The brassinosteroid (BR) biosynthetic gene, OsBR6ox, was the first BR biosynthetic gene isolated from monocots as the causal gene of the brd1 mutant, which exhibits a severe dwarf phenotype. Additionally BU1 and SG1 were found to positively and negatively regulate BR signaling, respectively. DPF, the causal gene of another lesion mimic mutant, was shown to regulate the transcription of diterpenoid phytoalexin biosynthetic genes. Furthermore, two BROAD-SPECTRUM RESISTANCE (BSR) genes were identified, which confer broad-spectrum disease resistance when overexpressed in multiple plant species. BSR1, which encodes a receptor-like cytoplasmic kinase, is involved in MAMP signaling, while BSR2, which encodes a cytochrome P450 protein, is associated with flower and seed size in addition to disease resistance.
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