期刊
VIRUSES-BASEL
卷 13, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/v13081447
关键词
tomato spotted wilt virus; Sw-5b; NLR receptor; plant innate immunity; defense signaling
类别
资金
- National Natural Science Foundation of China [31630062, 31925032, 31870143]
- Fundamental Research Funds for the Central Universities [JCQY202104, KYXK202012]
- Youth Science and Technology Innovation Program
The Sw-5b gene confers resistance to TSWV and encodes an NLR protein with a SD domain. The study identified the importance of the chaperone SGT1 in Sw-5b function and highlighted the independent role of EDS1 and NDR1 in Sw-5b-mediated immune signaling. Additionally, the study showed that NPR1 and NRCs are essential components in the Sw-5b signaling pathway, while ADR1 and NRG1 may not be involved in Sw-5b-mediated resistance to TSWV.
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.
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