A bacterial F-box effector suppresses SAR immunity through mediating the proteasomal degradation of OsTrxh2 in rice
A bacterial F-box effector suppresses SAR immunity through mediating the proteasomal degradation of OsTrxh2 in rice
复制标题
细菌 F-box 效应子通过介导水稻中 OsTrxh2 的蛋白酶体降解来抑制 SAR 免疫
DOI：
10.1111/tpj.14980
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发表时间：
2020-10-14
期刊：
影响因子：
7.2
通讯作者：
Li, Zongyun
中科院分区：
文献类型：
--
作者：
Ji, Hongtao;Liu, Delong;Li, Zongyun
植物病原菌通常通过分泌和转运大量的毒力效应物进入寄主细胞，抑制寄主的各种免疫途径而致病。已经证明，宿主细胞广泛的泛素系统经常通过各种策略被许多病原菌干扰或劫持。一些植物病原菌的III型分泌系统(T3SS)效应物为了自身的利益而模拟Skp1/CUL1/F-box(SCF)E3泛素系统的F-box蛋白(FBP)成分。尽管通过生物信息学分析已经筛选出许多与真核生物类似的F-box效应器，但大多数F-box效应器在宿主免疫系统中的靶点仍不清楚。在这里，我们发现XopI，一个可能的非洲Xoo(Xanthomonas oryzaepv.oryzae)菌株BAI3的F盒效应器，强烈抑制宿主对Xoo的OsNPR1依赖的抗性。ThexopI基因敲除突变体对水稻的致病力低于BAI3。从机制上讲，我们发现了一种硫氧还蛋白，OsTrxh2，它是水稻中的一种XopI相互作用蛋白。虽然OsTrxh2通过催化OsNPR1解离为水稻中的单体来积极调节水稻的免疫，但XopI效应器作为F-box适配器形成OSK1-XopI-OsTrxh2相互作用复合体，并通过蛋白酶体降解OsTrxh2进一步破坏OsNPR1介导的抗性。我们的结果表明，XopI以OsTrxh2为靶标，进一步抑制OsNPR1依赖的信号转导，从而破坏水稻的系统获得性抗性(SAR)免疫。
Plant bacterial pathogens usually cause diseases by secreting and translocating numerous virulence effectors into host cells and suppressing various host immunity pathways. It has been demonstrated that the extensive ubiquitin systems of host cells are frequently interfered with or hijacked by numerous pathogenic bacteria, through various strategies. Some type-III secretion system (T3SS) effectors of plant pathogens have been demonstrated to impersonate the F-box protein (FBP) component of the SKP1/CUL1/F-box (SCF) E3 ubiquitin system for their own benefit. Although numerous putative eukaryotic-like F-box effectors have been screened for different bacterial pathogens by bioinformatics analyses, the targets of most F-box effectors in host immune systems remain unknown. Here, we show that XopI, a putative F-box effector of AfricanXoo(Xanthomonas oryzaepv.oryzae) strain BAI3, strongly inhibits the host's OsNPR1-dependent resistance toXoo. ThexopIknockout mutant displays lower virulence inOryza sativa(rice) than BAI3. Mechanistically, we identify a thioredoxin protein, OsTrxh2, as an XopI-interacting protein in rice. Although OsTrxh2 positively regulates rice immunity by catalyzing the dissociation of OsNPR1 into monomers in rice, the XopI effector serves as an F-box adapter to form an OSK1-XopI-OsTrxh2 interaction complex, and further disrupts OsNPR1-mediated resistance through proteasomal degradation of OsTrxh2. Our results indicate that XopI targets OsTrxh2 and further represses OsNPR1-dependent signaling, thereby subverting systemic acquired resistance (SAR) immunity in rice.