ETI signaling nodes are involved in resistance of Hawaii 7996 to Ralstonia solanacearum-induced bacterial wilt disease in tomato

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.

KEYWORDS:

• Ralstonia solanacearum
• Hawaii 7996
• resistance mechanism
• effector-triggered immunity

Disclosure statement

No potential conflict of interest was reported by the authors.

Author contributions

B.L. designed and coordinated the entire project. A.X. performed experiments, data analysis and wrote the manuscript. L.W. helped with the VIGS assay. J.K. and C.F. generated the tomato mutant. P.L., C.F., and X.Y. analyzed data and provided critical feedback. B.L., A.X., and X.Y. participated in manuscript revision. All authors read and approved the manuscript.

Additional information

Funding

The research was supported by the National Natural Science Foundation of China [32272556, 31970125]; Pests and Diseases Green Prevention and Control Major Special Project [110202101045, LS-05]