Auxin transport inhibition precedes root nodule formation in white clover roots and is regulated by flavonoids and derivatives of chitin oligosaccharides
Auxin transport inhibition precedes root nodule formation in white clover roots and is regulated by flavonoids and derivatives of chitin oligosaccharides
复制标题
DOI：
10.1046/j.1365-313x.1998.00090.x
复制
发表时间：
1998-04-01
期刊：
影响因子：
7.2
通讯作者：
Djordjevic, MA
中科院分区：
文献类型：
--
作者：
Mathesius, U;Schlaman, HRM;Djordjevic, MA
在转基因白三叶草植物中检查生长素响应报告构建体 GH3:gusA 的表达，以评估根瘤形成最早阶段生长素平衡的变化。使用两种精确的接种技术：点接种和弹道微靶向的新方法，在施加细菌或信号分子后在标记位置监测报告基因表达。在接种豆科根瘤菌三叶根瘤菌、非宿主根瘤菌、脂甲壳寡糖 (LCO)、甲壳寡糖、合成生长素转运抑制剂（萘基邻苯二甲酸；NPA）、生长素、ENOD40-1 肽或不同黄酮类化合物后，监测 GH3:gusA 表达的变化。结果表明，三叶草结瘤根瘤菌在根瘤起始过程中诱导 GH3:gusA 表达快速、短暂和局部下调，随后在根瘤起始位点报告基因表达上调。生长素的微靶向导致 GH3:gusA 表达局部和顶部上调，而 NPA 导致局部和顶部表达下调。 R. I. 的点接种和微靶向。 trifolii LCO 或黄酮苷元诱导的 GH3:gusA 表达变化与 NPA 类似。 O-乙酰化甲壳寡糖引起 GH3:gusA 表达的变化与 R. I. 类似。 trifolii 点接种，但仅在通过微靶向递送后进行。非 O-乙酰化几丁质寡糖、类黄酮苷或 ENOD40-1 肽未能诱导 GH3:gusA 表达发生任何可检测的变化。根瘤和侧根发育后期的 GM:gusA 表达模式相似。这些结果支持这样的假设：LCO 和几丁质寡糖通过在根瘤形成的最早阶段扰乱根中的生长素流动而发挥作用，并且内源类黄酮可以介导这种反应。
The expression of the auxin responsive reporter construct, GH3:gusA, was examined in transgenic white clover plants to assess changes in the auxin balance during the earliest stages of root nodule formation. Reporter gene expression was monitored at marked locations after the application of bacteria or signal molecules using two precise inoculation techniques: spot-inoculation and a novel method for ballistic microtargeting. Changes in GH3:gusA expression were monitored after the inoculation of Rhizobium leguminosarum biovar trifolii, non-host rhizobia, lipo-chitin oligosaccharides (LCOs), chitin oligosaccharides, a synthetic auxin transport inhibitor (naphthylphthalamic acid; NPA), auxin, the ENOD40-1 peptide or different flavonoids. The results show that clover-nodulating rhizobia induce a rapid, transient and local downregulation of GH3:gusA expression during nodule initiation followed by an upregulation of reporter gene expression at the site of nodule initiation. Microtargeting of auxin caused a local and acropetal upregulation of GH3:gusA expression, whereas NPA caused local and acropetal downregulation of expression. Both spot-inoculation and microtargeting of R. I. by. trifolii LCOs or flavonoid aglycones induced similar changes to GH3:gusA expression as NPA. O-acetylated chitin oligosaccharides caused similar changes to GH3:gusA expression as R. I. by. trifolii spot-inoculation, but only after delivery by microtargeting. Non-O-acetylated chitin oligosaccharides, flavonoid glucosides or the ENOD40-1 peptide failed to induce any detectable changes in GH3:gusA expression. GM:gusA expression patterns during the later stages of nodule and lateral root development were similar. These results support the hypothesis that LCOs and chitin oligosaccharides act by perturbing the auxin flow in the root during the earliest stages of nodule formation, and that endogenous flavonoids could mediate this response.