State Key Laboratory of Soil and Sustainable Agriculture, Institute of Soil Science, Chinese Academy of Sciences, Nanjing, 210008, China.
School of Environment Science and Spatial Informatics, China University of Mining and Technology, Xuzhou, 221116, China.
Planta. 2024 Jan 30;259(3):52. doi: 10.1007/s00425-024-04331-3.
Auxin acts upstream of NO through NOA and XXT5 pathways to regulate the binding capacity of the root cell wall to Al. In our previous study, we identified an unknown mechanism by which 1-naphthaleneacetic acid (NAA) decreased the fixation of aluminum (Al) in the cell wall. Here, we observed that external application of the nitric oxide (NO) donor S-nitrosoglutathion (GSNO) increased the inhibition of Al on root elongation. Further analysis indicated that GSNO could induce Al accumulation in the roots and root cell walls, which is consistent with lower xyloglucan content. In comparison to the Columbia-0 (Col-0) wild type (WT), endogenous NO-reduced mutants noa1 (NOA pathway) and nia1nia2 (NR pathway) were more resistant to Al, with lower root Al content, higher xyloglucan content, and more Al accumulation in the root cell walls. By contrast, the xxt5 mutant with reduced xyloglucan content exhibited an Al-sensitive phenotype. Interestingly, Al treatment increased the endogenous auxin and NO levels, and the auxin levels induced under Al stress further stimulated NO production. Auxin application reduced Al retention in hemicellulose and decreased the xyloglucan content, similar to the effects observed with GSNO. In yucca and aux1-7 mutants, exogenous application of NO resulted in responses similar to those of the WT, whereas exogenous auxin had little effect on the noa1 mutant under Al stress. In addition, as auxin had similar effects on the nia1nia2 mutant and the WT, exogenous auxin and NO had little effect on the xxt5 mutant under Al stress, further confirming that auxin acts upstream of NO through NOA and XXT5 pathways to regulate the binding capacity of the root cell wall to Al.
生长素通过 NOA 和 XXT5 途径作用于 NO 上游,调节根细胞壁与 Al 的结合能力。在我们之前的研究中,我们发现了一个未知的机制,即 1-萘乙酸(NAA)降低细胞壁中 Al 的固定。在这里,我们观察到外施一氧化氮(NO)供体 S-亚硝基谷胱甘肽(GSNO)增加了 Al 对根伸长的抑制作用。进一步分析表明,GSNO 可以诱导 Al 在根和根细胞壁中的积累,这与木葡聚糖含量降低一致。与哥伦比亚-0(Col-0)野生型(WT)相比,内源 NO 还原突变体 noa1(NOA 途径)和 nia1nia2(NR 途径)对 Al 更具抗性,根 Al 含量较低,木葡聚糖含量较高,根细胞壁中 Al 积累较多。相比之下,木葡聚糖含量降低的 xxt5 突变体表现出 Al 敏感表型。有趣的是,Al 处理增加了内源生长素和 NO 水平,并且在 Al 胁迫下诱导的生长素水平进一步刺激了 NO 的产生。生长素的应用减少了 Al 在半纤维素中的保留,并降低了木葡聚糖的含量,这与 GSNO 观察到的效果相似。在丝兰和 aux1-7 突变体中,外源 NO 的应用导致与 WT 相似的反应,而在 Al 胁迫下,外源生长素对 noa1 突变体几乎没有影响。此外,由于生长素对 nia1nia2 突变体和 WT 具有相似的作用,因此在 Al 胁迫下,外源生长素和 NO 对 xxt5 突变体几乎没有影响,这进一步证实了生长素通过 NOA 和 XXT5 途径作用于 NO 上游,调节根细胞壁与 Al 的结合能力。