The Allelochemical MDCA Inhibits Lignification and Affects Auxin Homeostasis1[OPEN]
The Allelochemical MDCA Inhibits Lignification and Affects Auxin Homeostasis1[OPEN]
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DOI：
10.1104/pp.15.01972
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发表时间：
2016-08
期刊：
影响因子：
7.4
通讯作者：
Ward Steenackers;I. Cesarino;Petr Klíma;M. Quareshy;Ruben Vanholme;Sander Corneillie;Robert P. Kumpf;Dorien Van de Wouwer;K. Ljung;G. Goeminne;O. Novák;E. Zažímalová;R. Napier;W. Boerjan;B. Vanholme
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文献类型：
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作者：
Ward Steenackers;I. Cesarino;Petr Klíma;M. Quareshy;Ruben Vanholme;Sander Corneillie;Robert P. Kumpf;Dorien Van de Wouwer;K. Ljung;G. Goeminne;O. Novák;E. Zažímalová;R. Napier;W. Boerjan;B. Vanholme
植物来源的苯丙素途径抑制剂3，4-（亚甲二氧基）肉桂酸（MDCA）在拟南芥中的植物毒性是基于生长素稳态的扰动。苯丙素类化合物3，4-（亚甲二氧基）肉桂酸（MDCA）是首先从芦笋的根中提取的植物源化合物，并且进一步表征为化感物质。后来，MDCA被鉴定为4-香豆素-CoA连接酶（4CL）的有效抑制剂，4CL是一般苯丙烷途径的关键酶。通过阻断4CL，MDCA影响许多重要代谢物的生物合成，这可能解释其植物毒性。为了阐明MDCA化感活性的分子基础，我们评估了该化合物对拟南芥幼苗的影响。代谢谱显示，MDCA在植物体内转化为胡椒酸（PA），这是肉桂酸-4-羟化酶（C4 H）的抑制剂，C4 H是4CL的直接上游酶。C4 H的抑制作用也反映在MDCA处理的植物的酚类化合物中。处理在体外生长的植物导致抑制主根生长和增殖的侧根和不定根。这些观察到的生长缺陷不是木质素扰动的结果，而是干扰生长素稳态的结果。基于DII-VENUS定量和直接测量细胞生长素运输，我们得出结论，MDCA干扰生长素流出生长素梯度。此外，质谱分析显示MDCA触发生长素的生物合成、结合和催化。生长素稳态中的一个类似的转变，发现在C4 h突变体参考3 -2，表明MDCA触发的苯丙烷类和生长素的生物合成途径之间的串扰独立于所观察到的生长素流出抑制。总之，我们的数据提供，据我们所知，一个新的分子解释MDCA的植物毒性特性。
The phytotoxicity in Arabidopsis of the plant-derived phenylpropanoid pathway inhibitor 3,4-(methylenedioxy)cinnamic acid (MDCA) is based on the perturbation of auxin homeostasis. The phenylpropanoid 3,4-(methylenedioxy)cinnamic acid (MDCA) is a plant-derived compound first extracted from roots of Asparagus officinalis and further characterized as an allelochemical. Later on, MDCA was identified as an efficient inhibitor of 4-COUMARATE-CoA LIGASE (4CL), a key enzyme of the general phenylpropanoid pathway. By blocking 4CL, MDCA affects the biosynthesis of many important metabolites, which might explain its phytotoxicity. To decipher the molecular basis of the allelochemical activity of MDCA, we evaluated the effect of this compound on Arabidopsis thaliana seedlings. Metabolic profiling revealed that MDCA is converted in planta into piperonylic acid (PA), an inhibitor of CINNAMATE-4-HYDROXYLASE (C4H), the enzyme directly upstream of 4CL. The inhibition of C4H was also reflected in the phenolic profile of MDCA-treated plants. Treatment of in vitro grown plants resulted in an inhibition of primary root growth and a proliferation of lateral and adventitious roots. These observed growth defects were not the consequence of lignin perturbation, but rather the result of disturbing auxin homeostasis. Based on DII-VENUS quantification and direct measurement of cellular auxin transport, we concluded that MDCA disturbs auxin gradients by interfering with auxin efflux. In addition, mass spectrometry was used to show that MDCA triggers auxin biosynthesis, conjugation, and catabolism. A similar shift in auxin homeostasis was found in the c4h mutant ref3-2, indicating that MDCA triggers a cross talk between the phenylpropanoid and auxin biosynthetic pathways independent from the observed auxin efflux inhibition. Altogether, our data provide, to our knowledge, a novel molecular explanation for the phytotoxic properties of MDCA.