BioDiscovery Institute and Department of Biological Sciences, University of North Texas, Denton, TX 76203.
National Key Laboratory of Plant Molecular Genetics & CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai 200032, China.
Proc Natl Acad Sci U S A. 2021 Feb 2;118(5). doi: 10.1073/pnas.2010911118.
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 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 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) 的沉积和木质化既受季节性因素的影响，也受非生物胁迫的影响，而这些反应可能涉及激素脱落酸 (ABA)。然而，其中涉及的机制尚不清楚。在这里，我们表明通过涉及 SnRK2 激酶的核心 ABA 信号通路，限制 ABA 合成或信号转导的突变会减少 通过核心 ABA 信号通路，限制 ABA 合成或信号转导的突变会减少 的 SCW 厚度和木质化程度。SnRK2.2.3 和 6 与 SCW 调节因子 NAC 次生壁增厚促进因子 1 (NST1) 物理相互作用，NST1 是一个 NAC 家族转录因子，它协调一组下游 SCW 生物合成基因的转录激活，其中一些基因参与纤维素和木质素的生物合成。这种相互作用导致 NST1 在丝氨酸 316 处发生磷酸化，该残基在双子叶植物的 NST1 蛋白中高度保守，但在单子叶植物中不存在，并且是下游与 SCW 相关基因启动子转录激活所必需的。在 突变背景中 NST1 的功能丧失导致茎的居间纤维区域缺乏 SCWs，并且 NST1 的 Ser316Ala 突变体不能弥补这种表型和 ABA 诱导的木质素途径基因表达。发现 NST1 是 SnRK2 磷酸化的关键底物，这表明 ABA 介导的核心信号级联为陆生植物提供了一种激素调节的、具有竞争力的耐旱策略，使它们能够分化出由具有更厚细胞壁的细胞组成的输水和支持组织。
