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.

盐分严重影响植物生长并限制农业生产力。植物细胞壁的动态变化和重排是对盐胁迫的重要反应，但对特定细胞壁成分在反应中的生物学重要性知之甚少。在这里，我们展示了 β-1,4-半乳聚糖在盐过敏中的特定功能。我们发现盐胁迫通过上调编码 β-1,4-半乳聚糖合酶的GALACTAN SYNTHASE 1 ( GALS1 )的表达来诱导 β-1,4-半乳聚糖在根细胞壁中的积累。β-1,4-半乳聚糖的积累对耐盐性产生负面影响。D-半乳糖（D-Gal）的外源应用导致野生型和GALS1中 β-1,4-半乳聚糖水平的增加突变体，特别是在GALS1过表达子中，这与加重的盐过敏相关。此外，我们发现 BARLEY B RECOMBINANT/BASIC PENTACYSTEINE 转录因子 BPC1/BPC2 通过抑制GALS1表达和 β-1,4-半乳聚糖积累正向调节植物耐盐性。遗传分析表明GALS1在控制盐敏感性和 β-1,4-半乳聚糖积累方面对BPC1/BPC2具有遗传上位性。总之，我们的结果揭示了一种新的调控机制，通过该机制，受 BPC1/BPC2-GALS1 模块调控的 β-1,4-半乳聚糖会加剧拟南芥的盐敏感性。