Kang Guo, Daojun Li, Yan Li, Xiaoqing Wang, Chunfei Wang, Yanbin Zhu, Chengyun Wu, Zhubing Hu
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K<sup>+</sup> deprivation specifically leads to the accumulation of salicylic acid (SA) in the dlr1-1 mutant, consistent with the upregulation of SA biosynthesis genes. Moreover, exogenous application of SA to wild-type plants (B73) mimics the dlr1-1 phenotype. Conversely, treatment of the dlr1-1 mutant with 2-aminoindane-2-phosphonic acid, an SA biosynthesis inhibitor, partially restores LR emergence, indicating that elevated SA levels may be responsible for the mutant's developmental defects. MutMap analysis and allelism tests confirmed that the phenotypes of the dlr1-1 mutant results from the loss of the Na<sup>+</sup>/H<sup>+</sup> antiporter, ZmNHX7. Additionally, the application of NaCl exacerbates the dlr1-1 mutant phenotype, suggesting that the root defects in dlr1-1 mutant depend on ion homoeostasis. 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引用次数: 0
摘要
根系结构(RSA)是植物的一个重要性状,它决定了植物吸收水分和养分的能力。在这项研究中,我们描述了一种根系发育存在营养依赖性缺陷的突变体,它同时影响主根和侧根(LRs)。这种突变体是通过筛选 LR 发育缺陷而发现的,被命名为 dlr1-1。dlr1-1 突变体表现出 LR 出现障碍,而不是 LR 初级体(LRP)形成缺陷,尤其是在钾(K+)剥夺条件下。这种缺陷可能源于 dlr1-1 突变导致的细胞增殖抑制。钾(K+)剥夺会导致水杨酸(SA)在 dlr1-1 突变体中积累,这与 SA 生物合成基因的上调是一致的。此外,向野生型植株(B73)施用外源 SA 能模拟 dlr1-1 的表型。相反,用 2- 氨基茚满-2-膦酸(一种 SA 生物合成抑制剂)处理 dlr1-1 突变体,可部分恢复 LR 的萌发,这表明 SA 水平的升高可能是造成突变体发育缺陷的原因。MutMap 分析和等位基因测试证实,dlr1-1 突变体的表型是由于 Na+/H+ 反转运体 ZmNHX7 的缺失造成的。此外,施加 NaCl 会加剧 dlr1-1 突变体的表型,这表明 dlr1-1 突变体的根缺陷取决于离子平衡。总之,我们的研究结果表明,玉米 DLR1/NHX7 在钾匮乏条件下对根的发育至关重要。
Maize DLR1/NHX7 Is Required for Root Development Under Potassium Deficiency.
Root System Architecture (RSA) is a crucial plant trait that governs a plant's ability to absorb water and nutrients. In this study, we describe a mutant with nutrient-dependent defects in root development, affecting both the primary root and lateral roots (LRs). This mutant, identified through a screen for defects in LR development, has been designated dlr1-1. The dlr1-1 mutant exhibits impaired LR emergence rather than defects in the LR primordium (LRP) formation, particularly under potassium (K+)-deprivation conditions. This impairment likely stems from inhibited cell proliferation caused by the dlr1-1 mutation. K+ deprivation specifically leads to the accumulation of salicylic acid (SA) in the dlr1-1 mutant, consistent with the upregulation of SA biosynthesis genes. Moreover, exogenous application of SA to wild-type plants (B73) mimics the dlr1-1 phenotype. Conversely, treatment of the dlr1-1 mutant with 2-aminoindane-2-phosphonic acid, an SA biosynthesis inhibitor, partially restores LR emergence, indicating that elevated SA levels may be responsible for the mutant's developmental defects. MutMap analysis and allelism tests confirmed that the phenotypes of the dlr1-1 mutant results from the loss of the Na+/H+ antiporter, ZmNHX7. Additionally, the application of NaCl exacerbates the dlr1-1 mutant phenotype, suggesting that the root defects in dlr1-1 mutant depend on ion homoeostasis. In conclusion, our findings demonstrate that maize DLR1/NHX7 is essential for root development under potassium deprivation.
期刊介绍:
Plant, Cell & Environment is a premier plant science journal, offering valuable insights into plant responses to their environment. Committed to publishing high-quality theoretical and experimental research, the journal covers a broad spectrum of factors, spanning from molecular to community levels. Researchers exploring various aspects of plant biology, physiology, and ecology contribute to the journal's comprehensive understanding of plant-environment interactions.