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Wiley InterScience | ||
![]() The Plant JournalVolume 38 Issue 2, Pages 227 - 243 Published Online: 1 Mar 2004 Journal compilation © 2010 Blackwell Publishing Ltd and the Society for Experimental Biology Published in association with the Society for Experimental Biology
Abstract | References | Full Text: HTML, PDF (Size: 563K) | Related Articles | Citation Tracking A link between sterol biosynthesis, the cell wall, and cellulose in Arabidopsis Copyright © 2004 Blackwell Publishing Ltd KEYWORDS sterols • cellulose • cell wall • embryogenesis • GC–MS •
Arabidopsis
ABSTRACTA crucial role for sterols in plant growth and development is underscored by the identification of three Arabidopsis sterol biosynthesis mutants that exhibit embryonic defects: fackel (fk), hydra1 (hyd1), and sterol methyltransferase 1/cephalopod (smt1/cph). 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 hyd1 in comparison to fk reveals an abnormal accumulation of unique sterol intermediates in each case. Sterol profiling of the fk hyd1 double mutant provides genetic evidence that FK C-14 reductase acts upstream of HYD1 C-8,7 isomerase. Despite distinct differences in sterol profiles, fk and hyd1 as well as smt1/cph 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. Received 29 October 2003; revised 22 December 2003; accepted 23 December 2003. |