Cell wall β-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.

Salinity severely reduces plant growth and limits agricultural productivity. Dynamic changes and rearrangement of the plant cell wall is an important response to salt stress, but relatively little is known about the biological importance of specific cell wall components in the response. Here, we demonstrate a specific function of β-1,4-galactan in salt hypersensitivity. We found that salt stress induces the accumulation of β-1,4-galactan in root cell walls by up regulating the expression of GALACTAN SYNTHASE 1 (GALS1), which encodes a β-1,4-galactan synthase. The accumulation of β-1,4-galactan negatively affects salt tolerance. Exogenous application of D-galactose (D-Gal) causes an increase in β-1,4-galactan levels in the wild type and GALS1 mutants, especially in GALS1 overexpressors, which correlated with the aggravated salt hypersensitivity. Furthermore, we discovered that the BARLEY B RECOMBINANT/BASIC PENTACYSTEINE transcription factors BPC1/BPC2 positively regulate plant salt tolerance by repressing GALS1 expression and β-1,4-galactan accumulation. Genetic analysis suggested that GALS1 is genetically epistatic to BPC1/BPC2 with respect to the control of salt sensitivity as well as accumulation of β-1,4-galactan. Taken together, our results reveal a new regulatory mechanism by which β-1,4-galactan regulated by the BPC1/BPC2-GALS1 module aggravates salt sensitivity in Arabidopsis thaliana.