Ralstonia solanacearum Type III Effector RipAC Targets SGT1 to Suppress Effector-Triggered Immunity
Ralstonia solanacearum Type III Effector RipAC Targets SGT1 to Suppress Effector-Triggered Immunity
复制标题
DOI：
10.1093/pcp/pcaa122
复制
发表时间：
2020-12-01
影响因子：
4.9
通讯作者：
Mukaihara, Takafumi
中科院分区：
文献类型：
--
作者：
Nakano, Masahito;Ichinose, Yuki;Mukaihara, Takafumi
青枯雷尔氏菌（Ralstonia solanacearum）将III型效应子注射到宿主细胞中引起茄科植物的细菌性枯萎病。为了鉴别R.青枯菌效应子抑制植物中的效应子触发免疫（ETI），我们评估了R.在本发明的烟草中，由于其抑制由无毒（Avr）效应子RipAA诱导的过敏反应（HR）的能力，因此被认为是青枯菌RS1000效应子。在测试的11种效应物中，4种抑制RipAA触发的HR细胞死亡。其中，RipAC包含富含亮氨酸重复序列（LRR）基序的串联重复序列，其用作蛋白质-蛋白质相互作用的结构支架。我们发现RipAC的LRR结构域对于在识别RipAA和另一种Avr效应子RipP1期间抑制HR细胞死亡是不可或缺的。通过酵母双杂交筛选，我们鉴定了N。benthamiana SGT1，一种与RAR 1形成分子伴侣复合物的衔接蛋白，作为RipAC靶标的宿主因子。RipAC在酵母和植物细胞中与NbSGT1相互作用。在分子伴侣复合物形成后，RipAC的存在显著抑制了NbSGT1和NbRAR 1之间的相互作用。在NbSGT1沉默的植物中没有观察到RipAA和RipP1触发的HR细胞死亡。RipAC的引入是对R.青枯菌突变株。本萨米亚纳这些结果表明，R.青枯菌使用RipAC来破坏NbSGT1介导的分子伴侣复合物的形成，并在Avr效应物的识别过程中抑制ETI反应。
Ralstonia solanacearum injects type III effectors into host cells to cause bacterial wilt in Solanaceae plants. To identify R. solanacearum effectors that suppress effector-triggered immunity (ETI) in plants, we evaluated R. solanacearum RS1000 effectors for their ability to suppress a hypersensitive response (HR) induced by the avirulence (Avr) effector RipAA in Nicotiana benthamiana. Out of the 11 effectors tested, 4 suppressed RipAA-triggered HR cell death. Among them, RipAC contains tandem repeats of the leucine-rich repeat (LRR) motif, which serves as the structural scaffold for a protein-protein interaction. We found that the LRR domain of RipAC was indispensable for the suppression of HR cell death during the recognition of RipAA and another Avr effector RipP1. By yeast two-hybrid screening, we identified N. benthamiana SGT1, an adaptor protein that forms a molecular chaperone complex with RAR1, as a host factor of the RipAC target. RipAC interacted with NbSGT1 in yeast and plant cells. Upon the formation of the molecular chaperone complex, the presence of RipAC markedly inhibits the interaction between NbSGT1 and NbRAR1. The RipAA- and RipP1-triggered HR cell deaths were not observed in NbSGT1-silenced plants. The introduction of RipAC was complementary to the reduced growth of the R. solanacearum mutant strain in N. benthamiana. These findings indicate that R. solanacearum uses RipAC to subvert the NbSGT1-mediated formation of the molecular chaperone complex and suppress ETI responses during the recognition of Avr effectors.