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P23k is a monocot-unique protein that is highly expressed in barley. Our previous loss-of-function studies in barley leaves indicated that P23k, localized to tissues where cell wall polysaccharides accumulate, might contribute to secondary wall formation in the leaf. However, the P23k loss-of-function analysis was limited to the leaf, which is a vegetative organ. Considering the involvement of P23k in secondary wall formation, a dramatically altered phenotype is expected in the stem of P23k gene-silenced barley, where marked secondary wall deposition occurs during the reproductive growth stage. To test this hypothesis, barley striped mosaic virus-based virus-induced gene silencing of P23k was performed. Abnormal tiller formation and arrested intercalary elongation were observed in P23k-silenced barley. From these results, we speculated that cell wall architecture was altered by P23k gene silencing. Consistent with this idea, we observed a marked decrease in the amount of cell wall polysaccharides stained with calcofluor and down-regulation of the cellulose synthase-like CslF6 gene involved in (1,3;1,4)-β-D-glucan synthesis. Taken together, these results suggest that P23k is possibly involved in determining secondary wall architecture and contributes to tiller formation and intercalary elongation in barley.

Gene silencing of barley P23k involved in secondary wall formation causes abnormal tiller formation and intercalary elongation