Relocalization of Late Blight Resistance Protein R3a to Endosomal Compartments Is Associated with Effector Recognition and Required for the Immune Response
Relocalization of Late Blight Resistance Protein R3a to Endosomal Compartments Is Associated with Effector Recognition and Required for the Immune Response
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DOI：
10.1105/tpc.112.104992
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发表时间：
2012-12-01
期刊：
影响因子：
11.6
通讯作者：
Birch, Paul R. J.
中科院分区：
文献类型：
--
作者：
Engelhardt, Stefan;Boevink, Petra C.;Birch, Paul R. J.
植物-病原体相互作用研究的一个重要目标是确定抗性蛋白在何处检测病原体效应子以启动免疫应答。许多核苷结合-亮氨酸重复序列（NB-LRR）抗性蛋白在效应子识别后积累在植物细胞核中，在那里它们启动过敏反应（HR）。在这里，我们表明，马铃薯（马铃薯）抗性蛋白R3 a从细胞质中迁移到内体隔间只有当共表达公认的致病疫霉效应形式AVR 3a（KI），而不是未识别的形式AVR 3a（EM）。此外，AVR 3a（KI），而不是AVR 3a（EM），在R3 a存在下也重新定位于内体。R3 a和AVR 3a（KI）在植物核内体上物理位置非常接近。用布雷菲尔德菌素A（BFA）或渥曼青霉素（内吞周期抑制剂）处理，可以减弱R3 a在内体的重新定位和R3 a介导的HR。这些抑制剂对基因对Rx 1/PVX-CP和Sto 1/IpiO 1触发的HR没有观察到这样的影响。一个R3 a（D501 V）自激活的MHD突变体，在没有AVR 3a（KI）的情况下触发HR，未能定位到核内体。此外，BFA和渥曼青霉素没有改变这种突变体引发的细胞死亡。我们的结论是，NB-LRR抗性蛋白R3 a的效应识别和随后的HR信号需要其重新定位到内吞途径中的囊泡。
An important objective of plant-pathogen interactions research is to determine where resistance proteins detect pathogen effectors to mount an immune response. Many nucleotide binding-Leucine-rich repeat (NB-LRR) resistance proteins accumulate in the plant nucleus following effector recognition, where they initiate the hypersensitive response (HR). Here, we show that potato (Solanum tuberosum) resistance protein R3a relocates from the cytoplasm to endosomal compartments only when coexpressed with recognized Phytophthora infestans effector form AVR3a(KI) and not unrecognized form AVR3a(EM). Moreover, AVR3a(KI), but not AVR3a(EM), is also relocalized to endosomes in the presence of R3a. Both R3a and AVR3a(KI) colocalized in close physical proximity at endosomes in planta. Treatment with brefeldin A (BFA) or wortmannin, inhibitors of the endocytic cycle, attenuated both the relocalization of R3a to endosomes and the R3a-mediated HR. No such effect of these inhibitors was observed on HRs triggered by the gene-for-gene pairs Rx1/PVX-CP and Sto1/IpiO1. An R3a(D501V) autoactive MHD mutant, which triggered HR in the absence of AVR3a(KI), failed to localize to endosomes. Moreover, BFA and wortmannin did not alter cell death triggered by this mutant. We conclude that effector recognition and consequent HR signaling by NB-LRR resistance protein R3a require its relocalization to vesicles in the endocytic pathway.