Mutants of <i>Arabidopsis thaliana</i> with altered cell wall polysaccharide composition

Plant Journal - Tập 12 Số 2 - Trang 335-345 - 1997
Wolf‐Dieter Reiter1, Clint Chapple2, Chris Somerville3
1Department of Molecular and Cell Biology, and Institute of Materials Science, University of Connecticut, 75 North Eagleville Rd, Storrs, CT 06269,
2Department of Biochemistry, Purdue University, West Lafayette, IN 47907, and
3Department of Plant Biology, Carnegie Institution of Washington, Stanford, CA 94305, USA

Tóm tắt

To analyze the synthesis, structure and function of the plant cell wall by a genetic approach, 5200 chemically mutagenized Arabidopsis plants were screened for changes in the monosaccharide composition of hydrolyzed cell wall material by gas chromatography of alditol acetates. This screening procedure identified 23 mutant lines representing 11 different loci designated mur1 to mur11. The mur lines fall into essentially three groups: (1) complete absence of a monosaccharide, (2) significant reduction in the amount of a single monosaccharide, and (3) complex alterations in the relative amounts of several monosaccharides. All mutants in the first category represent alleles of the mur1 locus, and are deficient in the de novo synthesis of fucose. Mutants with reductions in a single monosaccharide have been identified for fucose (mur2, mur3), arabinose (mur4, mur5, mur6, mur7), and rhamnose (mur8). Mutants with complex changes in monosaccharide composition are represented by the mur9, mur10 and mur11 loci. Most of the mutant lines did not show obvious morphological or physiological alterations; however, lines mur1, mur9 and mur10 co‐segregated with reduced vigor or dwarfism of the plants. These results demonstrate the feasibility of identifying plants with altered cell wall compositions via a biochemical screening procedure. The availability of these mutants provides novel opportunities to study the functions of cell wall polysaccharides, gain insight into the biosynthesis of cell wall material, and clone cell wall‐related genes.

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