Monolignol biosynthesis is associated with resistance to Sclerotinia sclerotiorum in Camelina sativa
Eynck, C., Séguin-Swartz, G., Clarke, W.E., Parkin, I.A.P. (2012). Monolignol biosynthesis is associated with resistance to Sclerotinia sclerotiorum in Camelina sativa. Molecular Plant Pathology, [online] 13(8), 887-899. http://dx.doi.org/10.1111/j.1364-3703.2012.00798.x
The ascomycete Sclerotinia sclerotiorum is a necrotrophic plant pathogen with an extremely broad host range. It causes stem rot in Camelina sativa, a crucifer with great potential as an alternative oilseed crop. Lignification is a common phenomenon in the expression of resistance against necrotrophs, but the molecular mechanisms underlying this defence response are poorly understood. We present histochemical, gene expression and biochemical data investigating the role of monolignols in the resistance of C. sativa to S. sclerotiorum. Comparative studies with resistant and susceptible lines of C. sativa revealed substantial differences in constitutive transcript levels and gene regulation patterns for members of the gene family encoding cinnamoyl-CoA reductase (CCR), the first enzyme specifically committed to the synthesis of lignin monomers. These differences were associated with anatomical and metabolic factors. While the induction of CsCCR2 expression after inoculation with S. sclerotiorum was associated with the deposition of lignin mainly derived from guaiacyl monomers, high constitutive levels of CsCCR4 paralleled a high syringyl lignin content in healthy stems of resistant plants. The results provide evidence that plant cell wall strengthening plays a role in the resistance of C. sativa to S. sclerotiorum, and that both constitutive and inducible defence mechanisms contribute to reduced symptom development in resistant germplasm. This study provides the first characterization of quantitative resistance in C. sativa to S. sclerotiorum. © HER MAJESTY THE QUEEN IN RIGHT OF CANADA 2012. MOLECULAR PLANT PATHOLOGY © 2012 BSPP AND BLACKWELL PUBLISHING LTD.