Synergistic interactions of the plant cell death pathways induced by Phytophthora infestans Nep1-like protein PiNPP1.1 and INF1 elicitin
Synergistic interactions of the plant cell death pathways induced by Phytophthora infestans Nep1-like protein PiNPP1.1 and INF1 elicitin
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DOI：
10.1094/mpmi-19-0854
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发表时间：
2006-08-01
影响因子：
3.5
通讯作者：
Kamoun, Sophien
中科院分区：
文献类型：
--
作者：
Kanneganti, Thirumala-Devi;Huitema, Edgar;Kamoun, Sophien
细胞死亡在植物-微生物相互作用中起着无处不在的作用，因为它与敏感和抗性相互作用有关。在细菌、真菌和卵菌中发现了一类细胞死亡诱导蛋白，称为NEP1样蛋白(NLP)。这些蛋白质可引起多种双子叶植物的非特异性坏死。在这里，我们描述了来自卵菌科致病疫霉的NLP家族的三个成员(PiNPP1.1、PiNPP1.2和PiNPP1.3)。利用双元马铃薯X病毒载体进行农业侵染，我们证明了PiNPP1.1可以诱导烟草和寄主植物番茄的细胞死亡。表达分析表明，PiNPP1.1在侵染番茄的后期表达上调。我们比较了PINPP1.1和INF1 elicitin的坏死诱导活性，INF1 elicitin是一种在烟草中触发过敏反应的蛋白质。利用病毒诱导的基因沉默，我们发现PiNPP1.1诱导的细胞死亡依赖于泛素连接酶相关蛋白SGT1和热休克蛋白HSP90。此外，由PiNPP1.1而不是INF1引发的细胞死亡依赖于防御信号蛋白COI1、MEK2、NPR1和TGA2.2，这表明有不同的信号需求。PiNPP1.1和INF1在N.benthamiana中的联合表达导致了细胞死亡的增强，表明这两种细胞死亡反应之间存在协同作用。总之，这些结果指出了PiNPP1.1和INF1在植物中诱导的潜在的不同但相互作用的细胞死亡途径。
Cell death plays a ubiquitous role in plant-microbe interactions, given that it is associated with both susceptible and resistance interactions. A class of cell death-inducing proteins, termed Nep1-like proteins (NLPs), has been reported in bacteria, fungi, and oomycetes. These proteins induce nonspecific necrosis in a variety of dicotyledonous plants. Here, we describe three members of the NLP family from the oomycete Phytophthora infestans (PiNPP1.1, PiNPP1.2, and PiNPP1.3). Using agroinfection with a binary Potato virus X vector, we showed that PiNPP1.1 induces cell death in Nicotiana benthamiana and the host plant tomato. Expression analyses indicated that PiNPP1.1 is up-regulated during late stages of infection of tomato by R infestans. We compared PINPP1.1 necrosis-inducing activity to INF1 elicitin, a well-studied protein that triggers the hypersensitive response in Nicotiana spp. Using virus-induced gene silencing, we showed that the cell death induced by PiNPP1.1 is dependent on the ubiquitin ligase-associated protein SGT1 and the heat-shock protein HSP90. In addition, cell death triggered by PiNPP1.1 but not that by INF1 was dependent on the defense-signaling proteins COI1, MEK2, NPR1, and TGA2.2, suggesting distinct signaling requirements. Combined expression of PiNPP1.1 and INF1 in N. benthamiana resulted in enhanced cell death, suggesting synergistic interplay between the two cell-death responses. Altogether, these results point to potentially distinct but interacting cell-death pathways induced by PiNPP1.1 and INF1 in plants.