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Genetic complexity of cellulose synthase A gene function in Arabidopsis embryogenesis

Beeckman, T., Przemeck, G.K.H., Stamatiou, G., Lau, R., Terryn, N., Rycke, R. de., Inze, D., Berleth, T.
Plant physiology 2002 v.130 no.4 pp. 1883-1893
Arabidopsis thaliana, phenotype, cell growth, glycosyltransferases, seedlings, embryo (plant), plant proteins, cell division, amino acid sequences, mutants, nucleotide sequences, chemical constituents of plants, enzyme activity, plant morphology, seed development
The products of the cellulose synthase A (CESA) gene family are thought to function as isoforms of the cellulose synthase catalytic subunit, but for most CESA genes, the exact role in plant growth is still unknown. Assessing the function of individual CESA genes will require the identification of the null-mutant phenotypes and of the gene expression profiles for each gene. Here, we report that only four of 10 CESA genes, CESA1, CESA2, CESA3, and CESA9 are significantly expressed in the Arabidopsis embryo. We further identified two new mutations in the RADIALLY SWOLLEN1 (RSW1/CESA1) gene of Arabidopsis that obstruct organized growth in both shoot and root and interfere with cell division and cell expansion already in embryogenesis. One mutation is expected to completely abolish the enzymatic activity of RSW1(CESA1) because it eliminated one of three conserved Asp residues, which are considered essential for beta-glycosyltransferase activity. In this presumed null mutant, primary cell walls are still being formed, but are thin, highly undulated, and frequently interrupted. From the heart-stage onward, cell elongation in the embryo axis is severely impaired, and cell width is disproportionally increased. In the embryo, CESA1, CESA2, CESA3, and CESA9 are expressed in largely overlapping domains and may act cooperatively in higher order complexes. The embryonic phenotype of the presumed rsw1 null mutant indicates that the RSW1(CESA1) product has a critical, nonredundant function, but is nevertheless not strictly required for primary cell wall formation.