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  • Suppression of Arabidopsis GGLT 1 affects growth by reducing the L‐galactose content and borate cross‐linking of rhamnogalacturonan‐ II
Title: Suppression of Arabidopsis GGLT 1 affects growth by reducing the L‐galactose content and borate cross‐linking of rhamnogalacturonan‐ II
Summary

Boron 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 ofRG‐IIto 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 onRG‐IIstructure and cross‐linking and on the growth of plants in which the expression of aGDP‐sugar transporter (GONST3/GGLT1) has been reduced. In theGGLT1‐silenced plants the amount of L‐galactose in side‐chain A ofRG‐IIis reduced by up to 50%. This leads to a reduction in the extent ofRG‐IIcross‐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 themur1mutant, which also disruptsRG‐IIcross‐linking,GGLT1‐silenced plants display a loss of cell wall integrity under salt stress. We conclude thatGGLT1 is probably the primary GolgiGDP‐L‐galactose transporter, and providesGDP‐L‐galactose forRG‐IIbiosynthesis. We propose that the L‐galactose residue is critical forRG‐IIdimerization and for the stability of the borate cross‐link.

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NSF-PAR ID:
10077629
Author(s) / Creator(s):
 ;  ;  ;  ;  ;  ;  ;  ;  ;  ;  ;  
Publisher / Repository:
Wiley-Blackwell
Date Published:
Journal Name:
The Plant Journal
Volume:
96
Issue:
5
ISSN:
0960-7412
Page Range / eLocation ID:
p. 1036-1050
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
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