Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.
Plant pathogen effector utilizes host susceptibility factor NRL1 to degrade the immune regulator SWAP70.
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DOI：
10.1073/pnas.1808585115
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发表时间：
2018-08-14
影响因子：
11.1
通讯作者：
Birch PRJ
中科院分区：
文献类型：
--
作者：
He Q;Naqvi S;McLellan H;Boevink PC;Champouret N;Hein I;Birch PRJ
植物病原体，如臭名昭著的马铃薯疫病病原体，在活的植物细胞内传递效应物来促进疾病。最近的证据表明，在活的植物细胞内，一些效应器会与内源性的免疫负调节因子，即所谓的易感(S)因子有关。到目前为止，人们对效应器如何利用S因子来灭活免疫系统知之甚少。我们发现致病疫霉效应子Pi02860利用马铃薯StNRL1蛋白作为S因子，促进其靶向免疫正向调节因子StSWAP70进行蛋白酶体介导的降解。我们的结果表明，通过减少NRL1的活性或可获得性来保护StSWAP70不被降解，为减轻晚疫病提供了一种手段。植物病原体将效应物送入植物细胞以抑制免疫。虽然许多效应器使阳性免疫调节器失活，但其他效应器与免疫负性调节器有关：即所谓的易感(S)因素。病原体是如何利用S因子抑制免疫的，目前知之甚少。致病疫霉RXLR效应子Pi02860与寄主蛋白NRL1相互作用，NRL1是一种S因子，其活性抑制INF1引发的细胞死亡，是晚疫病所必需的。我们发现NRL1在酵母和植物中与一种名为SWAP70的鸟核苷酸交换因子相互作用。SWAP70与内小体结合，是一种正向免疫调节因子。病毒诱导的SWAP70基因沉默促进致病疫霉在烟草中的定植并损害ICD。相反，SWAP70的瞬时过表达降低了致病疫霉的感染，加速了ICD。Pi02860和NRL1单独或联合表达可导致蛋白酶体介导的SWAP70降解。SWAP70的降解可以通过沉默NRL1或通过突变Pi02860来取消其与NRL1的相互作用来阻止。NRL1是一种BTB结构域蛋白，预测形成CULLIN3泛素E3连接酶的底物接头成分。二聚化缺陷突变体NRL1NQ不能与SWAP70相互作用，但与Pi02860保持相互作用。NRL1NQ作为显性-负性突变体，在效应子Pi02860存在的情况下阻止SWAP70的降解，并减少致病疫霉的感染。重要的是，Pi02860增强了NRL1和SWAP70之间的联系，促进了蛋白酶体介导的后者的降解，从而抑制了免疫。防止SWAP70的降解是抗击晚疫病的一项战略。
Plant pathogens, such as the infamous potato blight agent Phytophthora infestans, deliver effectors inside living plant cells to promote disease. Recent evidence suggests that some effectors will associate with endogenous negative regulators of immunity, or so-called susceptibility (S) factors, inside living plant cells. To date, little is known about how effectors exploit S factors to inactivate the immune system. We discovered that P. infestans effector Pi02860 uses the potato StNRL1 protein as an S factor by promoting its ability to target a positive regulator of immunity, StSWAP70, for proteasome-mediated degradation. Our results reveal that protecting StSWAP70 from degradation by reducing the activity or availability of NRL1 provides a means to attenuate late blight disease. Plant pathogens deliver effectors into plant cells to suppress immunity. Whereas many effectors inactivate positive immune regulators, other effectors associate with negative regulators of immunity: so-called susceptibility (S) factors. Little is known about how pathogens exploit S factors to suppress immunity. Phytophthora infestans RXLR effector Pi02860 interacts with host protein NRL1, which is an S factor whose activity suppresses INF1-triggered cell death (ICD) and is required for late blight disease. We show that NRL1 interacts in yeast and in planta with a guanine nucleotide exchange factor called SWAP70. SWAP70 associates with endosomes and is a positive regulator of immunity. Virus-induced gene silencing of SWAP70 in Nicotiana benthamiana enhances P. infestans colonization and compromises ICD. In contrast, transient overexpression of SWAP70 reduces P. infestans infection and accelerates ICD. Expression of Pi02860 and NRL1, singly or in combination, results in proteasome-mediated degradation of SWAP70. Degradation of SWAP70 is prevented by silencing NRL1, or by mutation of Pi02860 to abolish its interaction with NRL1. NRL1 is a BTB-domain protein predicted to form the substrate adaptor component of a CULLIN3 ubiquitin E3 ligase. A dimerization-deficient mutant, NRL1NQ, fails to interact with SWAP70 but maintains its interaction with Pi02860. NRL1NQ acts as a dominant-negative mutant, preventing SWAP70 degradation in the presence of effector Pi02860, and reducing P. infestans infection. Critically, Pi02860 enhances the association between NRL1 and SWAP70 to promote proteasome-mediated degradation of the latter and, thus, suppress immunity. Preventing degradation of SWAP70 represents a strategy to combat late blight disease.
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影响因子：
16.6
作者：
Boevink PC;Wang X;McLellan H;He Q;Naqvi S;Armstrong MR;Zhang W;Hein I;Gilroy EM;Tian Z;Birch PRJ
通讯作者：
Birch PRJ
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作者：
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通讯作者：
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影响因子：
4
作者：
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影响因子：
7.2
作者：
Gilroy, Eleanor M.;Hein, Ingo;Birch, Paul R. J.
通讯作者：
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影响因子：
7.2
作者：
Liu, YL;Schiff, M;Dinesh-Kumar, SP
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