Abstract：
Bacterial wilt caused by the soil-borne pathogen Ralstonia solanacearum is a destructive disease of tomato. Tomato cultivar Hawaii 7996 is well-known for its stable resistance against R. solanacearum. 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 R. solanacearum GMI1000 infection. By employing virus-induced gene silencing (VIGS) and CRISPR/Cas9 technologies, we found that SlNRG1-silenced and SlADR1-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 R. solanacearum, SlEDS1, SlSAG101a/b, and SlPAD4 were essential for the immune signaling pathways in Hawaii 7996. Overall, our results suggested that robust resistance of Hawaii 7996 to R. solanacearum 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 R. solanacearum and will accelerate the breeding of tomatoes resilient to diseases.
摘要：
由土壤传播的病原体青枯病引起的青枯病是番茄的破坏性疾病。番茄品种Hawaii7996以其对S.solanacearum的稳定抗性而闻名。然而,夏威夷7996的抗病机制尚未揭示。这里,我们表明，Hawaii7996激活了根细胞死亡反应，并表现出比易感品种Moneymaker更强的防御基因诱导。通过使用病毒诱导的基因沉默（VIGS）和CRISPR/Cas9技术，我们发现SlNRG1沉默和SlADR1沉默/敲除突变体番茄部分或完全丧失了对青枯病的抗性，表明辅助NLRSlADR1和SlNRG1是效应子触发免疫（ETI）途径的关键节点，夏威夷7996阻力是必需的。此外,而SlNDR1对于夏威夷7996对青枯菌的抗性是可有可无的，SlEDS1,SlSAG101a/b,和SlPAD4对于夏威夷7996的免疫信号通路至关重要。总的来说,我们的结果表明,Hawaii7996对青枯菌的强抗性依赖于ETI信号通路的多个保守关键节点的参与.这项研究揭示了番茄对青枯菌抗性的分子机制，并将加速番茄抗病能力的培育。
