Beschreibung:
<jats:title>Summary</jats:title><jats:p>A crucial role for sterols in plant growth and development is underscored by the identification of three <jats:italic>Arabidopsis</jats:italic> sterol biosynthesis mutants that exhibit embryonic defects: <jats:italic>fackel</jats:italic> (<jats:italic>fk</jats:italic>), <jats:italic>hydra1</jats:italic> (<jats:italic>hyd1</jats:italic>), and <jats:italic>sterol methyltransferase 1/cephalopod</jats:italic> (<jats:italic>smt1/cph</jats:italic>). We have taken a dual approach of sterol profiling and ultrastructural analysis to investigate the primary defects underlying the mutant phenotypes. Comprehensive gas chromatography (GC)–MS analysis of <jats:italic>hyd1</jats:italic> in comparison to <jats:italic>fk</jats:italic> reveals an abnormal accumulation of unique sterol intermediates in each case. Sterol profiling of the <jats:italic>fk hyd1</jats:italic> double mutant provides genetic evidence that FK C‐14 reductase acts upstream of HYD1 C‐8,7 isomerase. Despite distinct differences in sterol profiles, <jats:italic>fk</jats:italic> and <jats:italic>hyd1</jats:italic> as well as <jats:italic>smt1/cph</jats:italic> share ultrastructural features such as incomplete cell walls and aberrant cell wall thickenings in embryonic and post‐embryonic tissues. The common defects are coupled with ectopic callose and lignin deposits. We show that all three mutants exhibit a deficiency in cellulose, but are not reduced in pectin and sugars of the cell wall and cytosol. The sterol biosynthesis inhibitors 15‐azasterol and fenpropimorph also cause cell wall gaps in dividing root cells and a reduction in bulk cellulose, corroborating that the cell wall abnormalities are due to altered sterol composition. Our results demonstrate that sterols are crucial for cellulose synthesis in the building of the plant cell wall.</jats:p>