Characterization of the Roles of SGT1/RAR1, EDS1/NDR1, NPR1, and NRC/ADR1/NRG1 in Sw-5b-Mediated Resistance to Tomato Spotted Wilt Virus.
Characterization of the Roles of SGT1/RAR1, EDS1/NDR1, NPR1, and NRC/ADR1/NRG1 in Sw-5b-Mediated Resistance to Tomato Spotted Wilt Virus.
复制标题
SGT1/RAR1、EDS1/NDR1、NPR1 和 NRC/ADR1/NRG1 在 Sw-5b 介导的番茄斑萎病毒抗性中的作用特征
DOI：
10.3390/v13081447
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发表时间：
2021-07-25
期刊：
影响因子：
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通讯作者：
Tao X
中科院分区：
文献类型：
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作者：
Chen Z;Wu Q;Tong C;Chen H;Miao D;Qian X;Zhao X;Jiang L;Tao X
番茄Sw-5b基因具有抗番茄斑枯病病毒(TSWV)的功能，编码富含亮氨酸重复序列(NLR)的N-末端茄科专一性结构域(SD)。虽然我们对Sw-5b如何识别病毒NSM激发子的了解有了很大的提高，但Sw-5b激活下游防御信号的过程仍有待阐明。在这项研究中，我们使用了一个基于烟草Rattle病毒(TRV)的病毒诱导基因沉默(VIGS)系统来研究SGT1/RAR1、EDS1/NDR1、NPR1和NRC/ADR1/NRG1基因在Sw-5b介导的信号通路中的作用。我们发现Sw-5b的功能需要分子伴侣SGT1，而辅助分子伴侣RAR1则不是。Sw-5b介导的免疫信号不依赖于EDS1和NDR1。沉默NPR1是SA信号转导的中心成分，但在转Sw-5b基因的本底夜蛾植株中并未导致TSWV的系统感染。辅助NLR NRCS(细胞死亡所需的NLR)是Sw-5b介导的对TSWV感染的系统抵抗所必需的。抑制NRC2/3/4降低了对Sw-5b的抗性。然而，辅助NLRs ADR1和NRG1可能不参与Sw-5b信号通路。沉默ADR1和/或NRG1基因不影响Sw-5b介导的对TSWV的抗性。我们的发现为Sw-5b介导的信号通路中对保守关键成分的需求提供了新的见解。
The tomato Sw-5b gene confers resistance to tomato spotted wilt virus (TSWV) and encodes a nucleotide-binding leucine-rich repeat (NLR) protein with an N-terminal Solanaceae-specific domain (SD). Although our understanding of how Sw-5b recognizes the viral NSm elicitor has increased significantly, the process by which Sw-5b activates downstream defense signaling remains to be elucidated. In this study, we used a tobacco rattle virus (TRV)-based virus-induced gene silencing (VIGS) system to investigate the roles of the SGT1/RAR1, EDS1/NDR1, NPR1, and NRC/ADR1/NRG1 genes in the Sw-5b-mediated signaling pathway. We found that chaperone SGT1 was required for Sw-5b function, but co-chaperone RAR1 was not. Sw-5b-mediated immune signaling was independent of both EDS1 and NDR1. Silencing NPR1, which is a central component in SA signaling, did not result in TSWV systemic infection in Sw-5b-transgenic N. benthamiana plants. Helper NLR NRCs (NLRs required for cell death) were required for Sw-5b-mediated systemic resistance to TSWV infection. Suppression of NRC2/3/4 compromised the Sw-5b resistance. However, the helper NLRs ADR1 and NRG1 may not participate in the Sw-5b signaling pathway. Silencing ADR1, NRG1, or both genes did not affect Sw-5b-mediated resistance to TSWV. Our findings provide new insight into the requirement for conserved key components in Sw-5b-mediated signaling pathways.