Rice monoculm mutation moc2, which inhibits outgrowth of the second tillers, is ascribed to lack of a fructose-1,6-bisphosphatase

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We characterized a rice monoculm mutant moc2, which showed significantly reduced tiller numbers, pale-green leaves, a reduced growth rate, and a consequent dwarf phenotype. The monoculm feature was attributed to a deficiency in the efficient outgrowth of tiller buds, although the moc2 mutant produced tiller buds. Inconsistent change was observed in the expression of genes involved in tiller bud outgrowth, suggesting that the moc2 mutant has a defective function necessary for the tiller bud outgrowth. The gene responsible for the moc2 mutant was mapped to a locus encoding cytosolic fructose-1,6-bisphosphatase 1 (FBP1), in which a Tos17 retrotransposon was inserted in exon 4. Reverse-transcription PCR for the FBP1 gene amplified a shorter transcript from the moc2 mutant than from the wild-type plant. The sequence of the shorter transcript revealed a deletion of exon 4 by abnormal splicing, and the resulting frameshift generated a new translation termination signal. The moc2 mutant showed a very low level of FBPase activity, suggesting that it involves a loss-of-function mutation of FBP1. Cytosolic FBPase is considered a key enzyme in the sucrose biosynthesis pathway. Defective FBPase activity is anticipated to lead a shortage of sucrose supply, which probably causes the inhibition of tiller bud outgrowth in the moc2 mutant. The monoculm phenotype of the moc2 mutant supports the idea that sucrose supply may be an important cue to outgrow tiller buds.