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果胶甲酯酶抑制剂增强了对枯萎病的抗性。

A Pectin Methylesterase Inhibitor Enhances Resistance to Wilt.

机构信息

College of Science, China Agricultural University, Beijing 100193, China.

State Key Laboratory of Cotton Biology, Institute of Cotton Research of the Chinese Academy of Agricultural Sciences, Anyang 455000, China.

出版信息

Plant Physiol. 2018 Mar;176(3):2202-2220. doi: 10.1104/pp.17.01399. Epub 2018 Jan 23.

DOI:10.1104/pp.17.01399
PMID:29363564
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5841709/
Abstract

Pectins are major components of the primary plant cell wall, which functions as the primary barrier against pathogens. Pectin methylesterases (PMEs) catalyze the demethylesterification of the homogalacturonan domains of pectin in the plant cell wall. Their activity is regulated by PME inhibitors (PMEIs). Here, we provide evidence that the pectin methylesterase-inhibiting protein GhPMEI3 from cotton () functions in plant responses to infection by the fungus GhPMEI3 interacts with PMEs and regulates the expression of a specific fungal polygalacturonase (VdPG1). Ectopic expression of GhPMEI3 increased pectin methyl esterification and limited fungal disease in cotton, while also modulating root elongation. Enzymatic analyses revealed that GhPMEI3 efficiently inhibited the activity of cotton GhPME2/GhPME31. Experiments using transgenic Arabidopsis () plants expressing the gene under the control of the CaMV 35S promoter revealed that GhPMEI3 inhibits the endogenous PME activity in vitro. Moreover, the enhanced resistance to was associated with altered expression. Virus-induced silencing of resulted in increased susceptibility to Further, we investigated the interaction between GhPMEI3 and GhPME2/GhPME31 using inhibition assays and molecular docking simulations. The peculiar structural features of GhPMEI3 were responsible for the formation of a 1:1 stoichiometric complex with GhPME2/GhPME31. Together, these results suggest that GhPMEI3 enhances resistance to wilt. Moreover, GhPMEI3-GhPMEs interactions would be needed before drawing the correlation between structure-function and are crucial for plant development against the ever-evolving fungal pathogens.

摘要

果胶是植物初生细胞壁的主要成分,它是抵御病原体的第一道屏障。果胶甲酯酶(PMEs)催化果胶中半乳糖醛酸域的去甲酯化。其活性受 PME 抑制剂(PMEIs)调节。在这里,我们提供的证据表明,棉花中的果胶甲酯酶抑制蛋白 GhPMEI3 在植物对真菌的感染反应中发挥作用GhPMEI3 与 PMEs 相互作用并调节特定真菌多聚半乳糖醛酸酶(VdPG1)的表达。GhPMEI3 的异位表达增加了果胶甲酯化程度,限制了棉花的真菌病害,同时也调节了根的伸长。酶分析表明,GhPMEI3 有效地抑制了棉花 GhPME2/GhPME31 的活性。使用在 CaMV 35S 启动子控制下表达基因的转基因拟南芥()植物进行的实验表明,GhPMEI3 在体外抑制内源性 PME 活性。此外,增强的对 的抗性与改变的表达有关。通过病毒诱导的沉默使对的敏感性增加进一步,我们通过抑制测定和分子对接模拟研究了 GhPMEI3 与 GhPME2/GhPME31 之间的相互作用。GhPMEI3 的特殊结构特征负责与 GhPME2/GhPME31 形成 1:1 化学计量的复合物。总之,这些结果表明 GhPMEI3 增强了对枯萎病的抗性。此外,在得出结构-功能之间的相关性之前,需要 GhPMEI3-GhPMEs 相互作用,这对于植物发育至关重要,因为真菌病原体在不断进化。

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