Grass cell walls have a role in the inherent tolerance of grasses to the cellulose biosynthesis inhibitor isoxaben.

Abstract

Cellulose biosynthesis inhibitors (CBIs) are pre-emergence herbicides that inhibit anisotropic cell expansion resulting in a severely swollen and stunted growth phenotype. Resistance to group 21 CBIs, such as isoxaben, is conferred by missense mutations in CELLOSE SYNTHASE A (CesA) genes required for primary cell wall synthesis, concluding that this is their in vivo target. Herein, we show that grasses exhibit tolerance to group 21 CBIs and explore the mechanism of tolerance to isoxaben in the grass Brachypodium distachyon (L.). Comparative genomics failed to identify synonymous point mutations that have been found to confer isoxaben resistance in the dicot Arabidopsis thaliana (L.). Brachypodium did not metabolize 14 C-isoxaben. We next explored the role of grass-specific non-cellulosic cell wall components, specifically the hemicellulose polysaccharide mix linkage glucans (MLG), as a potential tolerance mechanism by compensating for the loss of cellulose during cell elongation. A partial-transcriptional knockdown T-DNA insertion was found in a key MLG synthesis gene, Cellulose synthase-like F6 (CslF6) and this mutant was found to be 2.1 times more sensitive to isoxaben than wild-type plants. These data suggest that the composition and compensatory response of grass cell walls may be a factor in conferring tolerance to group 21 CBIs. © 2017 Society of Chemical Industry.