1. Transcriptomic and physiological analyses reveal plant resistance against Ralstonia solanacearum involves salicylic acid‐mediated defences in tomato leaves.
- Author
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Li, Na, Sun, Sheng, Kong, Lingjuan, Chen, Zhifeng, Xin, Yidong, Shao, Renguang, Wang, Lumei, Wang, Hehe, and Geng, Xueqing
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BACTERIAL wilt diseases , *RALSTONIA solanacearum , *SALICYLIC acid , *PLANT disease treatment , *PHYTOPATHOGENIC microorganisms , *CELLULAR signal transduction - Abstract
The destructive bacterial wilt disease caused by Ralstonia solanacearum leads to substantial losses in tomato production worldwide. RNA‐seq is a powerful technology to decipher various biological processes of host–pathogen interactions by analysing differentially expressed genes (DEGs). In the current study, we used RNA‐seq to analyse the transcriptome changes during the interaction of R. solanacearum and susceptible tomato leaves at the time point of 24 h. Gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were used to annotate functions of DEGs in tomato plants. DEGs related to plant and pathogen interaction pathways, photosynthesis pathways and hormone signalling pathways were further analysed. Our results revealed that R. solanacearum inoculation activated plant defence response pathways to induce a number of core defence genes against bacterial invasion, inhibited expression of genes related to photosynthesis processes and activated the salicylic acid (SA) signalling pathway to induce defence responses. We quantified SA and jasmonic acid (JA) contents after bacterial inoculation. SA treatment alleviated plant disease symptoms and induced immune‐related reactive oxygen species (ROS) bursts in tomato leaves. The extent of disease symptoms was much greater in SlNPR1‐silenced plants than wild‐type plants. Together, our results will provide a better understanding of the mechanisms of plant induced defences against bacterial invasion and provide a theoretical basis for breeding resistance of tomato against R. solanacearum in future. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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