Present addresses: Bayer BioScience NV, TechnologiePark 58, Gent 9052, Belgium.
Cell wall glucomannan in Arabidopsis is synthesised by CSLA glycosyltransferases, and influences the progression of embryogenesis
Article first published online: 5 AUG 2009
© 2009 The Authors. Journal compilation © 2009 Blackwell Publishing Ltd
The Plant Journal
Volume 60, Issue 3, pages 527–538, November 2009
How to Cite
Goubet, F., Barton, C. J., Mortimer, J. C., Yu, X., Zhang, Z., Miles, G. P., Richens, J., Liepman, A. H., Seffen, K. and Dupree, P. (2009), Cell wall glucomannan in Arabidopsis is synthesised by CSLA glycosyltransferases, and influences the progression of embryogenesis. The Plant Journal, 60: 527–538. doi: 10.1111/j.1365-313X.2009.03977.x
- Issue published online: 28 OCT 2009
- Article first published online: 5 AUG 2009
- Received 27 April 2009; revised 22 June 2009; accepted 1 July 2009; published online 5 August 2009.
- cell wall
Mannans are hemicellulosic polysaccharides that have previously been implicated as structural constituents of cell walls and as storage reserves but which may serve other functions during plant growth and development. Several members of the Arabidopsis cellulose synthase-like A (CSLA) family have previously been shown to synthesise mannan polysaccharides in vitro when heterologously expressed. It has also been found that CSLA7 is essential for embryogenesis, suggesting a role for the CSLA7 product in development. To determine whether the CSLA proteins are responsible for glucomannan synthesis in vivo, we characterised insertion mutants in each of the nine Arabidopsis CSLA genes and several double and triple mutant combinations. csla9 mutants showed substantially reduced glucomannan, and triple csla2csla3csla9 mutants lacked detectable glucomannan in stems. Nevertheless, these mutants showed no alteration in stem development or strength. Overexpression of CSLA2, CSLA7 and CSLA9 increased the glucomannan content in stems. Increased glucomannan synthesis also caused defective embryogenesis, leading to delayed development and occasional embryo death. The embryo lethality of csla7 was complemented by overexpression of CSLA9, suggesting that the glucomannan products are similar. We conclude that CSLA2, CSLA3 and CSLA9 are responsible for the synthesis of all detectable glucomannan in Arabidopsis stems, and that CSLA7 synthesises glucomannan in embryos. These results are inconsistent with a substantial role for glucomannan in wall strength in Arabidopsis stems, but indicate that glucomannan levels affect embryogenesis. Together with earlier heterologous expression studies, the glucomannan deficiency observed in csla mutant plants demonstrates that the CSLA family encodes glucomannan synthases.