Plant secondary cell-wall (SCW) deposition and lignification are affected by both seasonal factors and abiotic stress, and these responses may involve the hormone abscisic acid (ABA). However, the mechanisms involved are not clear. Here we show that mutations that limit ABA synthesis or signaling reduce the extent of SCW thickness and lignification in Arabidopsis thaliana through the core ABA-signaling pathway involving SnRK2 kinases. SnRK2.2. 3 and 6 physically interact with the SCW regulator NAC SECONDARY WALL THICKENING PROMOTING FACTOR 1 (NST1), a NAC family transcription factor that orchestrates the transcriptional activation of a suite of downstream SCW biosynthesis genes, some of which are involved in the biosynthesis of cellulose and lignin. This interaction leads to phosphorylation of NST1 at Ser316, a residue that is highly conserved among NST1 proteins from dicots, but not monocots, and is required for transcriptional activation of downstream SCW-related gene promoters. Loss of function of NST1 in the snd1 mutant background results in lack of SCWs in the interfascicular fiber region of the stem, and the Ser316Ala mutant of NST1 fails to complement this phenotype and ABA-induced lignin pathway gene expression. The discovery of NST1 as a key substrate for phosphorylation by SnRK2 suggests that the ABA-mediated core-signaling cascade provided land plants with a hormone-modulated, competitive desiccation-tolerance strategy allowing them to differentiate water-conducting and supporting tissues built of cells with thicker cell walls.

植物次生细胞壁（SCW）的沉积和木质化受季节因素和非生物胁迫的影响，这些响应可能涉及脱落酸（ABA）。但是，涉及的机制尚不清楚。在这里我们表明，限制ABA合成或信号传导的突变降低了拟南芥中SCW厚度和木质化的程度通过涉及SnRK2激酶的核心ABA信号通路。SnRK2.2。3和6与SCW调节剂NAC次级壁增厚促进因子1（NST1）发生物理相互作用，NAC家族转录因子可协调一系列下游SCW生物合成基因的转录激活，其中一些基因参与了纤维素和木质素。这种相互作用导致NST1在Ser316处磷酸化，该残基在双子叶植物的NST1蛋白中高度保守，而单子叶植物不是，并且是下游SCW相关基因启动子转录激活所必需的。snd1中NST1的功能丧失突变体背景导致茎的束间纤维区域中缺少SCW，NST1的Ser316Ala突变体无法补充这种表型和ABA诱导的木质素途径基因表达。NST1作为SnRK2磷酸化的关键底物的发现表明，ABA介导的核心信号级联反应为陆地植物提供了一种激素调节的，竞争性的耐干燥性策略，从而使它们能够区分水传导细胞和支持细胞的组织较厚的细胞壁。