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ETI 信号节点参与了番茄 Hawaii 7996 对细菌性萎蔫病的抗性。

ETI signaling nodes are involved in resistance of Hawaii 7996 to bacterial wilt disease in tomato.

机构信息

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, Hubei, China.

The Provincial Key Lab of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, Hubei, China.

出版信息

Plant Signal Behav. 2023 Dec 31;18(1):2194747. doi: 10.1080/15592324.2023.2194747.

DOI:10.1080/15592324.2023.2194747
PMID:36994774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10072054/
Abstract

Bacterial wilt caused by the soil-borne pathogen is a destructive disease of tomato. Tomato cultivar Hawaii 7996 is well-known for its stable resistance against . However, the resistance mechanism of Hawaii 7996 has not yet been revealed. Here, we showed that Hawaii 7996 activated root cell death response and exhibited stronger defense gene induction than the susceptible cultivar Moneymaker after GMI1000 infection. By employing virus-induced gene silencing (VIGS) and CRISPR/Cas9 technologies, we found that -silenced and -silenced/knockout mutant tomato partially or completely lost resistance to bacterial wilt, indicating that helper NLRs SlADR1 and SlNRG1, the key nodes of effector-triggered immunity (ETI) pathways, are required for Hawaii 7996 resistance. In addition, while SlNDR1 was dispensable for the resistance of Hawaii 7996 to , SlEDS1, SlSAG101a, and SlPAD4 were essential for the immune signaling pathways in Hawaii 7996. Overall, our results suggested that robust resistance of Hawaii 7996 to relied on the involvement of multiple conserved key nodes of the ETI signaling pathways. This study sheds light on the molecular mechanisms underlying tomato resistance to and will accelerate the breeding of tomatoes resilient to diseases.

摘要

由土壤病原菌引起的细菌性萎蔫病是番茄的一种毁灭性疾病。番茄品种 Hawaii 7996 以其对 的稳定抗性而闻名。然而,Hawaii 7996 的抗性机制尚未被揭示。在这里,我们发现与易感品种 Moneymaker 相比,Hawaii 7996 在 GMI1000 感染后激活了根细胞死亡反应,并表现出更强的防御基因诱导。通过采用病毒诱导的基因沉默 (VIGS) 和 CRISPR/Cas9 技术,我们发现沉默和沉默/敲除突变体番茄部分或完全丧失了对细菌性萎蔫病的抗性,表明辅助 NLRs SlADR1 和 SlNRG1 是效应触发免疫 (ETI) 途径的关键节点,是 Hawaii 7996 抗性所必需的。此外,虽然 SlNDR1 对 Hawaii 7996 对 的抗性是可有可无的,但 SlEDS1、SlSAG101a 和 SlPAD4 是 Hawaii 7996 免疫信号通路所必需的。总体而言,我们的研究结果表明,Hawaii 7996 对 的强大抗性依赖于 ETI 信号通路的多个保守关键节点的参与。本研究揭示了番茄对 的抗性的分子机制,并将加速对疾病具有抗性的番茄的培育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/471d49de6d09/KPSB_A_2194747_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/9ff59c060030/KPSB_A_2194747_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/c432a97fdba7/KPSB_A_2194747_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/94485041066d/KPSB_A_2194747_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/5d6e893aa68d/KPSB_A_2194747_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/ffb22e947824/KPSB_A_2194747_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/471d49de6d09/KPSB_A_2194747_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/9ff59c060030/KPSB_A_2194747_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/c432a97fdba7/KPSB_A_2194747_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/94485041066d/KPSB_A_2194747_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/5d6e893aa68d/KPSB_A_2194747_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/ffb22e947824/KPSB_A_2194747_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8240/10072054/471d49de6d09/KPSB_A_2194747_F0006_OC.jpg

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