Suppression of Arabidopsis GGLT1 affects growth by reducing the L-galactose content and borate cross-linking of rhamnogalacturonan-II.

Abstract

SummaryBoron is a micronutrient that is required for the normal growth and development of vascular plants, but its precise functions remain a subject of debate. One established role for boron is in the cell wall where it forms a diester cross‐link between two monomers of the low‐abundance pectic polysaccharide rhamnogalacturonan‐II (RG‐II). The inability of RG‐II to properly assemble into a dimer results in the formation of cell walls with abnormal biochemical and biomechanical properties and has a severe impact on plant productivity. Here we describe the effects on RG‐II structure and cross‐linking and on the growth of plants in which the expression of a GDP‐sugar transporter (GONST3/GGLT1) has been reduced. In the GGLT1‐silenced plants the amount of L‐galactose in side‐chain A of RG‐II is reduced by up to 50%. This leads to a reduction in the extent of RG‐II cross‐linking in the cell walls as well as a reduction in the stability of the dimer in the presence of calcium chelators. The silenced plants have a dwarf phenotype, which is rescued by growth in the presence of increased amounts of boric acid. Similar to the mur1 mutant, which also disrupts RG‐II cross‐linking, GGLT1‐silenced plants display a loss of cell wall integrity under salt stress. We conclude that GGLT1 is probably the primary Golgi GDP‐L‐galactose transporter, and provides GDP‐L‐galactose for RG‐II biosynthesis. We propose that the L‐galactose residue is critical for RG‐II dimerization and for the stability of the borate cross‐link.