Abstract
Solanum melongena L. (eggplant) bacterial wilt is a severe soil borne disease. Here, this study aimed to explore the regulation mechanism of eggplant bacterial wilt-resistance by transcriptomics with weighted gene co-expression analysis network (WGCNA). The different expression genes (DEGs) of roots and stems were divided into 21 modules. The module of interest (root: indianred4, stem: coral3) with the highest correlation with the target traits was selected to elucidate resistance genes and pathways. The selected module of roots and stems co-enriched the pathways of MAPK signalling pathway, plant pathogen interaction, and glutathione metabolism. Each top 30 hub genes of the roots and stems co-enriched a large number of receptor kinase genes. A total of 14 interesting resistance-related genes were selected and verified with quantitative polymerase chain reaction (qPCR). The qPCR results were consistent with those of WGCNA. The hub gene of EGP00814 (namely SmRPP13L4) was further functionally verified; SmRPP13L4 positively regulated the resistance of eggplant to bacterial wilt by qPCR and virus-induced gene silencing (VIGS). Our study provides a reference for the interaction between eggplants and bacterial wilt and the breeding of broad-spectrum and specific eggplant varieties that are bacterial wilt-resistant.
Highlights
Solanum melongena L. bacterial wilt is a devastating soil borne disease caused by Ralstonia solanacearum that severely restricts the growth, yield, and production of eggplants
China produces the highest amount of eggplants, which are widely cultivated throughout the country
The nucleotide-binding leucine-rich repeat (NLR) protein family of intracellular immune receptors binds to the pathogen and triggers the second anti-epidemic effector-triggered immunity (ETI) of plant cells
Summary
Solanum melongena L. (eggplant) bacterial wilt is a devastating soil borne disease caused by Ralstonia solanacearum that severely restricts the growth, yield, and production of eggplants. R. solanacearum mainly invades natural orifices and wounds of roots before rapidly proliferating in the xylem and spreading to the stem During this process, the pathogen induces change in the walls and membranes of the cells, deposits callose, produces lipopolysaccharide, and blocks catheters, thereby leading to plant wilting. The nucleotide-binding leucine-rich repeat (NLR) protein family of intracellular immune receptors binds to the pathogen and triggers the second anti-epidemic effector-triggered immunity (ETI) of plant cells. This is accompanied by hypersensitivity reaction (HR), changes in defence-related gene expression, production of mitogen-activated protein phosphorylated kinase (MAPK) and plant hormone [3,4,5], and induction of systemic acquired resistance (SAR). To further interpret the regulatory mechanism in eggplant bacterial wilt-resistance and screen the varieties with broad-spectrum resistance to bacterial wilt more rapidly, gene mapping and transcriptome sequencing have been widely adopted
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