SRC2-1 is required in PcINF1-induced pepper immunity by acting as an interacting partner of PcINF1
SRC2-1 is required in PcINF1-induced pepper immunity by acting as an interacting partner of PcINF1
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SRC2-1 作为 PcINF1 的相互作用伙伴，是 PcINF1 诱导的辣椒免疫所必需的
DOI：
10.1093/jxb/erv161
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发表时间：
2015-07-01
影响因子：
6.9
通讯作者：
He, Shui-lin
中科院分区：
文献类型：
--
作者：
Liu, Zhi-qin;Qiu, Ai-lian;He, Shui-lin
激发素是可以在大多数烟草属中引发过敏性细胞死亡的激发子，但其潜在的分子机制还不清楚。对辣椒疫霉（Phytophthora capsici）诱导素基因PcINF 1进行了研究。PcINF 1瞬时过表达引发辣椒细胞死亡并伴随着超敏反应标志物超敏诱导反应基因1（HIR 1）和发病相关基因SAR 82、DEF 1、BPR 1和PO 2的上调。利用酵母双杂交技术从辣椒cDNA文库中筛选到一个与PcINF 1相互作用的蛋白SRC 2 -1，该蛋白定位于细胞膜。通过双分子荧光互补和免疫共沉淀证实了PcINF 1和SRC 2 -1之间的相互作用。辣椒植株中SRC 2 -1和PcINF 1的同时瞬时过表达引发了强烈的细胞死亡，而通过病毒诱导的基因沉默来沉默SRC 2 -1则阻断了PcINF 1诱导的细胞死亡，并增加了辣椒植株对辣椒疫霉感染的易感性。此外，细胞死亡诱导需要PcINF 1-SRC 2 -1复合物的膜靶向。SRC 2 -1的C2结构域对于SRC 2 -1质膜靶向和PcINF 1-SRC 2 -1相互作用至关重要。这些结果表明，SRC 2 -1与PcINF 1相互作用，并在PcINF 1诱导的辣椒免疫所需的。
Elicitins are elicitors that can trigger hypersensitive cell death in most Nicotiana spp., but their underlying molecular mechanism is not well understood. The gene Phytophthora capsici INF1 (PcINF1) coding for an elicitin from P. capsici was characterized in this study. Transient overexpression of PcINF1 triggered cell death in pepper (Capsicum annuum L.) and was accompanied by upregulation of the hypersensitive response marker, Hypersensitive Induced Reaction gene 1 (HIR1), and the pathogenesis-related genes SAR82, DEF1, BPR1, and PO2. A putative PcINF1-interacting protein, SRC2-1, was isolated from a pepper cDNA library by yeast two-hybrid screening and was observed to target the plasma membrane. The interaction between PcINF1 and SRC2-1 was confirmed by bimolecular fluorescence complementation and co-immunoprecipitation. Simultaneous transient overexpression of SRC2-1 and PcINF1 in pepper plants triggered intensive cell death, whereas silencing of SRC2-1 by virus-induced gene silencing blocked the cell death induction of PcINF1 and increased the susceptibility of pepper plants to P. capsici infection. Additionally, membrane targeting of the PcINF1-SRC2-1 complex was required for cell death induction. The C2 domain of SRC2-1 was crucial for SRC2-1 plasma membrane targeting and the PcINF1-SRC2-1 interaction. These results suggest that SRC2-1 interacts with PcINF1 and is required in PcINF1-induced pepper immunity.