The potato cyst nematode effector RHA1B is a ubiquitin ligase and uses two distinct mechanisms to suppress plant immune signaling
The potato cyst nematode effector RHA1B is a ubiquitin ligase and uses two distinct mechanisms to suppress plant immune signaling
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马铃薯胞囊线虫效应子 RHA1B 是一种泛素连接酶，使用两种不同的机制来抑制植物免疫信号传导
DOI：
10.1371/journal.ppat.1007720
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发表时间：
2019-04-01
期刊：
影响因子：
6.7
通讯作者：
Xiao, Fangming
中科院分区：
文献类型：
--
作者：
Kud, Joanna;Wang, Wenjie;Xiao, Fangming
植物病原体，如细菌、真菌、卵菌和线虫，依赖广泛的毒力效应物进入寄主细胞来抑制植物免疫。虽然植物细菌效应器已被广泛研究，但对植物寄生线虫效应器的功能知之甚少，如苍白球囊线虫，一种在马铃薯和番茄产业中造成巨大损失的孢囊线虫。在这里，我们利用体内和体外泛素化实验证明了马铃薯胞囊线虫(Globodera Pallida)效应子RHA1B是一种E3泛素连接酶，它利用多个宿主植物E2泛素连接酶来催化泛素化。RHA1B能够抑制效应触发免疫(ETI)，表现为抑制广泛的核苷酸结合富含亮氨酸重复序列(NB-LRR)免疫受体介导的超敏反应(HR)，可能是通过依赖于E3对NB-LRR受体的降解。RHA1B还阻断了flg22触发的Acre31和WRKY22的表达，这是病原体相关分子模式(PAMP)触发的免疫(PTI)的标志基因，但这不需要RHA1B的E3活性。此外，过量表达RHA1B基因的转基因马铃薯对灰霉病菌的感受性增强。因此，我们的数据表明，RHA1B不仅通过触发NB-LRR免疫受体的降解来阻断ETI信号，而且通过一种未知的E3非依赖机制抑制PTI信号，从而促进线虫寄生。
Plant pathogens, such as bacteria, fungi, oomycetes and nematodes, rely on wide range of virulent effectors delivered into host cells to suppress plant immunity. Although phytobacterial effectors have been intensively investigated, little is known about the function of effectors of plant-parasitic nematodes, such as Globodera pallida, a cyst nematode responsible for vast losses in the potato and tomato industries. Here, we demonstrate using in vivo and in vitro ubiquitination assays the potato cyst nematode (Globodera pallida) effector RHA1B is an E3 ubiquitin ligase that employs multiple host plant E2 ubiquitin conjugation enzymes to catalyze ubiquitination. RHA1B was able to suppress effector-triggered immunity (ETI), as manifested by suppression of hypersensitive response (HR) mediated by a broad range of nucleotide-binding leucine-rich repeat (NB-LRR) immune receptors, presumably via E3-dependent degradation of the NB-LRR receptors. RHA1B also blocked the flg22-triggered expression of Acre31 and WRKY22, marker genes of pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI), but this did not require the E3 activity of RHA1B. Moreover, transgenic potato overexpressing the RHA1B transgene exhibited enhanced susceptibility to G. pallida. Thus, our data suggest RHA1B facilitates nematode parasitism not only by triggering degradation of NB-LRR immune receptors to block ETI signaling but also by suppressing PTI signaling via an as yet unknown E3-independent mechanism.