Abstract

In the current study, we used a grapevine cell line in which actin filaments are labeled by GFP to show that aluminum causes actin remodeling through activation of NADPH oxidase in the plasma membrane, followed by activation of phytoalexin synthesis genes. Elimination of actin filaments by latrunculin B disrupts gene activation and inhibition of MAPK signaling by the inhibitor PD98059. Interestingly, aluminum also induces the transcription of ISOCHORISMATE SYNTHASE, a key enzyme for the synthesis of salicylic acid, as well as PR1, a gene that is known to be responsive to salicylic acid. However, while salicylic acid responses are usually a hallmark of the hypersensitive response, aluminum-triggered defense is not accompanied by cell death. Both actin remodeling and gene activation in response to aluminum can be suppressed by the natural auxin indole acetic acid, suggesting that the actin response is not caused by nonspecific signaling. Further evidence for the specificity of the aluminum-triggered activation of phytoalexin synthesis genes comes from experiments in which plant peptide elicitors induce significant cellular mortality but do not evoke induction of these transcription. The response in grapevine cells can be recapitulated in grapevine leaf discs from two genotypes contrasting in stilbene inducibility. Here, aluminum can induce accumulation of the central grapevine phytoalexin, the stilbene aglycone trans-resveratrol; this is preceded by a rapid induction of transcription for RESVERATROL SYNTHASE and the regulating transcription factor MYB14. The amplitude of this induction reflects the general stilbene inducibility of these genotypes, indicating that the aluminum effect is not caused by nonspecific toxicity but by activation of specific signaling pathways. The findings are discussed in relation to a model in which actin filaments activate a specific branch of defense signaling, acting in concert with calcium-dependent PAMP-triggered immunity. This pathway links the apoplastic oxidative burst through MAPK signaling with the activation of defense-related transcription.

中文翻译：

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铝可以通过肌动蛋白重塑激活葡萄树防御

 抽象的

在当前的研究中，我们使用了肌动蛋白丝被 GFP 标记的葡萄细胞系，表明铝通过激活质膜中的 NADPH 氧化酶，然后激活植物抗毒素合成基因，引起肌动蛋白重塑。 latrunculin B 消除肌动蛋白丝会破坏基因激活和抑制剂 PD98059 对 MAPK 信号传导的抑制。有趣的是，铝还诱导异分支酸合成酶（水杨酸合成的关键酶）以及PR1 （已知对水杨酸有反应的基因）的转录。然而，虽然水杨酸反应通常是过敏反应的标志，但铝触发的防御并不伴随细胞死亡。天然生长素吲哚乙酸可以抑制肌动蛋白重塑和响应铝的基因激活，这表明肌动蛋白反应不是由非特异性信号传导引起的。铝触发的植物抗毒素合成基因激活的特异性的进一步证据来自于实验，其中植物肽诱导子诱导显着的细胞死亡，但不引起这些转录的诱导。葡萄树细胞中的反应可以在两种二苯乙烯诱导能力对比的基因型的葡萄树叶盘中重现。在这里，铝可以诱导葡萄树中央植物抗毒素（二苯乙烯苷元反式白藜芦醇）的积累；在此之前，白藜芦醇合成酶和调节转录因子MYB14会快速诱导转录。 这种诱导的幅度反映了这些基因型的一般二苯乙烯诱导能力，表明铝效应不是由非特异性毒性引起的，而是由特定信号通路的激活引起的。讨论的结果与一个模型有关，在该模型中，肌动蛋白丝激活防御信号的特定分支，与钙依赖性 PAMP 触发的免疫协同作用。该途径通过 MAPK 信号传导将质外体氧化爆发与防御相关转录的激活联系起来。