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Exogenous application of histone demethylase inhibitor trans-2-phenylcyclopropylamine mimics FLD loss-of-function phenotype in terms of systemic acquired resistance in Arabidopsis thaliana

机译:就拟南芥的系统获得性抗性而言外源应用组蛋白脱甲基酶抑制剂反式-2-苯基环丙胺模拟FLD功能丧失表型

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摘要

Plants often learn from previous infections to mount higher level of resistance during subsequent infections, a phenomenon referred to as systemic acquired resistance (SAR). During primary infection, mobile signals generated at the infection site subsequently move to the rest of plant to activate SAR. SAR activation is associated with alteration in the nucleosomal composition at the promoters of several defense-related genes. However, genetic regulations of such epigenetic modifications are largely obscure. Recently, we have demonstrated that Reduced Systemic immunity1/FLOWERING LOCUS D (RSI1; alias FLD) a homolog of human histone demethylase, is required for SAR development in Arabidopsis. Here, we report that exogenous application of a histone demethylase inhibitor trans-2-phenylcyclopropylamine (2-PCPA) mimics rsi1/fld loss-of-function phenotypes in terms of SAR and associated histone demethylation at the promoters of PR1, WRKY 29, and WRKY6 genes, and as well as flowering phenotypes. Our results suggest histone demethylase activity of FLD is important for controlling SAR activation.
机译:植物通常会从先前的感染中学习,以在随后的感染中获得更高水平的抗性,这种现象称为系统性获得性抗性(SAR)。在初次感染期间,在感染部位产生的移动信号随后移至植物的其余部分以激活SAR。 SAR激活与几个防御相关基因的启动子上的核小体组成的改变有关。然而,这种表观遗传修饰的遗传调控在很大程度上是模糊的。最近,我们已经证明,拟南芥SAR的发展需要降低全身免疫力1 / FLOWERING LOCUS D(RSI1;别名FLD)人组蛋白脱甲基酶的同源物。在这里,我们报告说,组蛋白脱甲基酶抑制剂反式-2-苯基环丙胺(2-PCPA)的外源应用在SAR和PR1,WRKY 29和启动子的相关组蛋白去甲基化方面模拟了rsi1 / fld功能丧失表型。 WRKY6基因,以及开花表型。我们的结果表明FLD的组蛋白脱甲基酶活性对于控制SAR激活很重要。

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