Structure-function analysis of barley NLR immune receptor MLA10 reveals its cell compartment specific activity in cell death and disease resistance.

Structure-function analysis of barley NLR immune receptor MLA10 reveals its cell compartment specific activity in cell death and disease resistance.
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大麦 NLR 免疫受体 MLA10 的结构功能分析揭示了其在细胞死亡和抗病方面的细胞区室特异性活性

DOI:
10.1371/journal.ppat.1002752
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发表时间:
2012
期刊:
影响因子:
6.7
通讯作者:
Shen QH
Shen QH
中科院分区:
医学1区
文献类型:
--
作者:
Bai S;Liu J;Chang C;Zhang L;Maekawa T;Wang Q;Xiao W;Liu Y;Chai J;Takken FL;Schulze-Lefert P;Shen QH

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植物细胞内免疫受体包含大量类似于动物 NOD 样受体 (NLR) 的多结构域蛋白。植物 NLR 通常识别由无毒 (AVR) 基因编码的分离株特异性病原体衍生效应子,并触发通常与局部宿主细胞死亡相关的防御反应。大麦 MLA 基因本质上是多态性的,编码卷曲螺旋 (CC)-NB-LRR 类型的 NLR,每个 NLR 检测大麦白粉病真菌的同源分离株特异性效应子。我们报告了大麦和本塞姆氏烟草中 MLA10 抗病性和细胞死亡信号传导活性的系统分析。 MLA10 CC 结构域触发的细胞死亡受到 CC 和 NB-ARC 结构域中高度保守的基序以及受体 C 端 LRR 的调节。通过用核定位序列 (NLS) 或核输出序列 (NES) 进行标记,强制 MLA10 亚细胞定位表明细胞死亡信号传导中的 MLA10 活性在细胞核中受到抑制,但在细胞质中增强。相比之下,核定位的 MLA10 足以介导白粉病真菌的抗病性。 MLA10 在细胞质中的保留是通过附着糖皮质激素受体激素结合域 (GR) 来实现的,通过这种结构,我们增强了细胞质 MLA10 在细胞死亡信号传导中的作用。结合我们的数据显示,MLA10 细胞核在抗病性方面具有必要且充分的活性,这表明 MLA10 触发的细胞死亡和抗病信号以隔室依赖性方式存在分歧。
Plant intracellular immune receptors comprise a large number of multi-domain proteins resembling animal NOD-like receptors (NLRs). Plant NLRs typically recognize isolate-specific pathogen-derived effectors, encoded by avirulence (AVR) genes, and trigger defense responses often associated with localized host cell death. The barley MLA gene is polymorphic in nature and encodes NLRs of the coiled-coil (CC)-NB-LRR type that each detects a cognate isolate-specific effector of the barley powdery mildew fungus. We report the systematic analyses of MLA10 activity in disease resistance and cell death signaling in barley and Nicotiana benthamiana. MLA10 CC domain-triggered cell death is regulated by highly conserved motifs in the CC and the NB-ARC domains and by the C-terminal LRR of the receptor. Enforced MLA10 subcellular localization, by tagging with a nuclear localization sequence (NLS) or a nuclear export sequence (NES), shows that MLA10 activity in cell death signaling is suppressed in the nucleus but enhanced in the cytoplasm. By contrast, nuclear localized MLA10 is sufficient to mediate disease resistance against powdery mildew fungus. MLA10 retention in the cytoplasm was achieved through attachment of a glucocorticoid receptor hormone-binding domain (GR), by which we reinforced the role of cytoplasmic MLA10 in cell death signaling. Together with our data showing an essential and sufficient nuclear MLA10 activity in disease resistance, this suggests a bifurcation of MLA10-triggered cell death and disease resistance signaling in a compartment-dependent manner.
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