Os03g0416200

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Annotated Information

Mutation

• Compared to the cortical Wber cell walls of the wild-type Kinmaze internodes showing uniform thickness with a smooth surface on the cytoplasmic side (Fig. 1c), the sclerenchyma secondary cell wall of the mutant internodes had uneven thickness with a rough surface on the cytoplasmic side, resulting in a mixture of thin layers and irregular architecture (Fig. 1c). Therefore, we deWned this novel mutant as the cell wall architecture1 (cwa1) mutant. The cwa1 mutant plant had similar growth to the wildtypeKinmaze plant (Fig. 1a) and showed a morphologicallynormal tissue structure (Fig. 1b). However, the mutantexhibited a brittle culm phenotype with dramaticallyreduced mechanical strength in its tissue (supplementalFigure S1), implying improper formation of the secondarycell wall.

Fig. 1 Phenotypes of the wild-type and cwa1 mutant plants. a Mature wild-type (left) and cwa1 (right) plants showing almost the same height. b Cross-sections of the wild-type (left) and cwa1 (right) internodes showing no diVerence in morphology. c Under high magniWcation, the cwa1 cortical Wbers (right) show amorphous secondary cell walls. CF cortical Wber, LVB large vascular bundle, Pa fundamental parenchyma, SVB small vascular bundle. Bars 20 cm (a), 50 μm (b), 5 μm (c) .

• To examine at which point the amorphous cell wall of the cwa1 mutant develops, we compared the cortical Wber cell wall in the wild-type and cwa1 internodes at diVerent developmental stages. Just after cessation of internode elongation, slightly thickened secondary cell walls of wildtype cortical Wbers were observed by light microscopy, suggesting that secondary cell wall formation had already started (Fig. 2a); similar patterns were observed in cwa1 internodes at this stage. Then, the wild-type secondary cell wall began to thicken more uniformly during secondary cell wall synthesis (Fig. 2b). At almost the same stage, slight lesser extent than that for the wild-type (Fig. 2b). Notably, abnormal and irregularly thick regions were also observed in the same cwa1 cell wall (Fig. 2b, arrowheads), resulting in the formation of an amorphous secondary cell wall with uneven thickness. Such uneven cell wall structure in the cwa1 internodes was more prominent at the late stage of cell wall formation (Fig. 2c). In longitudinal sections of cwa1 internodes, both irregularly thick and thin regions were also clearly seen within the same sclerenchyma cell (Fig. 2d, e), although no diVerences in length or width were found between the cwa1 and wild-type sclerenchyma cells. These observations indicate marked disruption of secondary cell wall thickening of cwa1 sclerenchyma following normal cell expansion and elongation.

Fig. 2 Light microscopic images of abnormal secondary cell walls of the cwa1 internodes. .

Labs working on this gene

• Graduate School of Bio-Applications and Systems Engineering, Tokyo University of Agriculture and Technology, Koganei 184-8588, Japan
• College of Bioresource Science, Nihon University, 1866 Kameino, Fujisawa, Kanagawa 252-0880, Japan
• Forestry Research Institute, Oji Paper Co. Ltd, 24-9 Nobono-cho, Kameyama, Mie 519-0212, Japan
• Graduate School of Agriculture, Tokyo University of Agriculture and Technology, Fuchu 183-8538, Japan
• Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan
• Bioscience and Biotechnology Center, Nagoya University, Nagoya 464-8601, Japan