植物細(xì)胞內(nèi)抗病蛋白特異性識別病原菌后激發(fā)強(qiáng)烈的抗病反應(yīng)，這類抗病反應(yīng)往往伴有局部的細(xì)胞死亡。但抗病蛋白介導(dǎo)的抗病與細(xì)胞死亡的因果關(guān)系多有爭議,、其亞細(xì)胞分區(qū)定位與死亡信號的關(guān)系也不是很清楚。
中科院遺傳與發(fā)育生物學(xué)研究所沈前華課題組系統(tǒng)地研究了大麥白粉菌抗病蛋白MLA10結(jié)構(gòu)與功能的關(guān)系，亞細(xì)胞定位與抗病反應(yīng),、細(xì)胞死亡的關(guān)系等,。他們發(fā)現(xiàn),，由N端的Coiled-coil（CC）結(jié)構(gòu)域介導(dǎo)的細(xì)胞死亡受到精細(xì)的調(diào)控,，包括多個保守基序和C端LRR結(jié)構(gòu)域的調(diào)控,；也需要分子伴侶組份SGT1,、HSP90的參與,。
通過借助本生煙草（N. benthamiana）表達(dá)系統(tǒng)結(jié)合大麥中的抗病功能研究，結(jié)果表明細(xì)胞核內(nèi)MLA10足以限制白粉菌的生長,，但不引發(fā)細(xì)胞死亡,；而細(xì)胞質(zhì)中的MLA10能夠引發(fā)細(xì)胞死亡,。該研究揭示了MLA10介導(dǎo)細(xì)胞死亡信號與抗病信號的亞細(xì)胞功能分區(qū),，并提出抗病蛋白可能通過整合來自不同亞細(xì)胞區(qū)域的多種信號途徑,，最終達(dá)到有效抗病的目的,。
該研究結(jié)果近期發(fā)表在寄主與病原菌互作領(lǐng)域國際刊物PLoS pathogens上,。沈前華實驗室的博士生白世偉是該論文的第一作者,。該研究得到了科技部973計劃、國家自然科學(xué)基金委和中國科學(xué)院的資助，并得到國內(nèi)國際同行的協(xié)作,。（生物谷Bioon.com）
doi:10.1371/journal.ppat.1002752
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Structure-Function Analysis of Barley NLR Immune Receptor MLA10 Reveals Its Cell Compartment Specific Activity in Cell Death and Disease Resistance
Shiwei Bai1,2, Jie Liu1,2, Cheng Chang1,2, Ling Zhang1, Takaki Maekawa3, Qiuyun Wang1, Wenkai Xiao1, Yule Liu4, Jijie Chai4, Frank L. W. Takken5,6, Paul Schulze-Lefert3, Qian-Hua Shen1*
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.
