植物细胞内抗病蛋白特异性识别病原菌后激发强烈的抗病反应,这类抗病反应往往伴有局部的细胞死亡。但抗病蛋白介导的抗病与细胞死亡的因果关系多有争议、其亚细胞分区定位与死亡信号的关系也不是很清楚。
中科院遗传与发育生物学研究所沈前华课题组系统地研究了大麦白粉菌抗病蛋白MLA10结构与功能的关系,亚细胞定位与抗病反应、细胞死亡的关系等。他们发现,由N端的Coiled-coil(CC)结构域介导的细胞死亡受到精细的调控,包括多个保守基序和C端LRR结构域的调控;也需要分子伴侣组份SGT1、HSP90的参与。
通过借助本生烟草(N. benthamiana)表达系统结合大麦中的抗病功能研究,结果表明细胞核内MLA10足以限制白粉菌的生长,但不引发细胞死亡;而细胞质中的MLA10能够引发细胞死亡。该研究揭示了MLA10介导细胞死亡信号与抗病信号的亚细胞功能分区,并提出抗病蛋白可能通过整合来自不同亚细胞区域的多种信号途径,最终达到有效抗病的目的。
该研究结果近期发表在寄主与病原菌互作领域国际刊物PLoS pathogens上。沈前华实验室的博士生白世伟是该论文的第一作者。该研究得到了科技部973计划、国家自然科学基金委和中国科学院的资助,并得到国内国际同行的协作。(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.