Balanced nuclear and cytoplasmic activities of EDS1 are required for a complete plant innate immune response.
Balanced nuclear and cytoplasmic activities of EDS1 are required for a complete plant innate immune response.
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DOI：
10.1371/journal.ppat.1000970
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发表时间：
2010-07-01
期刊：
影响因子：
6.7
通讯作者：
Parker JE
中科院分区：
文献类型：
--
作者：
García AV;Blanvillain-Baufumé S;Huibers RP;Wiermer M;Li G;Gobbato E;Rietz S;Parker JE
植物对适应宿主的病原体的先天免疫的一个重要层是由识别特定微生物效应子的细胞内核苷酸结合/寡聚化结构域富含亮氨酸重复序列 (NB-LRR) 受体赋予的。来自 TIR（Toll/Interleukin-1 受体）-NB-LRR 类激活受体的信号汇聚到核质免疫调节因子 EDS1（疾病易感性增强1）上。在本报告中，我们表明受体刺激的核 EDS1 积累增加先于或同时发生于 EDS1 依赖性防御相关基因的诱导和抑制。 EDS1 能够通过核转运受体介导在细胞质和细胞核之间穿梭。通过在转基因拟南芥中增强 EDS1 从细胞核内部的输出（通过附加额外的核输出序列（NES））或有条件地将 EDS1 释放到细胞核（通过与糖皮质激素受体（GR）融合），我们确定 EDS1 核池对于抵抗生物营养和半生物营养病原体以及转录重编程至关重要。有证据表明转录后过程调节受体触发的 EDS1 在细胞核中的积累。核 EDS1 水平的变化与细胞质 EDS1 池达到平衡，并且需要细胞质 EDS1 来完全抵抗和限制感染位点的宿主细胞死亡。我们认为 EDS1 协调的核和细胞质活性使植物能够对病原体攻击产生适当平衡的免疫反应。植物已经进化出多层先天免疫系统来识别和应对环境中潜在的破坏性微生物。对侵入性生物营养型和半生物营养型病原体的抵抗通常涉及防御的转录动员和感染部位宿主细胞的程序性死亡。然而，这些过程会干扰正常的新陈代谢和生长，因此必须严格控制。在这项研究中，我们研究了病原体激活细胞内免疫受体后拟南芥细胞内的耐药信号传导事件。我们发现核质蛋白 EDS1 通过诱导和抑制特定的防御相关基因，充当免疫反应中转录重编程的重要调节因子。我们提供的证据表明，EDS1 通过细胞质和细胞核中的协调活动来实现其作为防御信号“枢纽”的作用。维持这两个 EDS1 库之间的平衡可能对于一系列传染性微生物的抵抗力和细胞死亡很重要，并且避免“过度”防御激活，这对植物有害。
An important layer of plant innate immunity to host-adapted pathogens is conferred by intracellular nucleotide-binding/oligomerization domain-leucine rich repeat (NB-LRR) receptors recognizing specific microbial effectors. Signaling from activated receptors of the TIR (Toll/Interleukin-1 Receptor)-NB-LRR class converges on the nucleo-cytoplasmic immune regulator EDS1 (Enhanced Disease Susceptibility1). In this report we show that a receptor-stimulated increase in accumulation of nuclear EDS1 precedes or coincides with the EDS1-dependent induction and repression of defense-related genes. EDS1 is capable of nuclear transport receptor-mediated shuttling between the cytoplasm and nucleus. By enhancing EDS1 export from inside nuclei (through attachment of an additional nuclear export sequence (NES)) or conditionally releasing EDS1 to the nucleus (by fusion to a glucocorticoid receptor (GR)) in transgenic Arabidopsis we establish that the EDS1 nuclear pool is essential for resistance to biotrophic and hemi-biotrophic pathogens and for transcriptional reprogramming. Evidence points to post-transcriptional processes regulating receptor-triggered accumulation of EDS1 in nuclei. Changes in nuclear EDS1 levels become equilibrated with the cytoplasmic EDS1 pool and cytoplasmic EDS1 is needed for complete resistance and restriction of host cell death at infection sites. We propose that coordinated nuclear and cytoplasmic activities of EDS1 enable the plant to mount an appropriately balanced immune response to pathogen attack. Plants have evolved a multilayered innate immune system to recognize and respond to potentially destructive microbes in the environment. Resistance to invasive biotrophic and hemi-biotrophic pathogens often involves transcriptional mobilization of defenses and programmed death of host cells at infection sites. However, these processes disturb normal metabolism and growth and therefore have to be tightly controlled. In this study, we examine resistance signaling events inside Arabidopsis cells after pathogen activation of intracellular immune receptors. We show that the nucleo-cytoplasmic protein EDS1 acts as an important regulator of transcriptional reprogramming in the immune response by allowing the induction and repression of particular defense-related genes. We provide evidence that EDS1 accomplishes its role as a defense signaling ‘hub’ through coordinated activities in the cytoplasm and nucleus. Maintaining a balance between these two EDS1 pools is probably important for resistance and cell death to a range of infectious microbes and to not ‘overshoot’ defense activation which would be detrimental for the plant.
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影响因子：
64.5
作者：
Caplan, Jeffrey L.;Mamillapalli, Padmavathi;Dinesh-Kumar, S. P.
通讯作者：
Dinesh-Kumar, S. P.
影响因子：
64.8
作者：
Lipford, JR;Smith, GT;Deshaies, RJ
通讯作者：
Deshaies, RJ
影响因子：
3.5
作者：
Li, X;Clarke, JD;Dong, XN
通讯作者：
Dong, XN
影响因子：
9.8
作者：
Burch-Smith TM;Schiff M;Caplan JL;Tsao J;Czymmek K;Dinesh-Kumar SP
通讯作者：
Dinesh-Kumar SP
影响因子：
7.2
作者：
Clough, SJ;Bent, AF
通讯作者：
Bent, AF