# A Comparative Transcriptome and WGCNA of Tomato Reveals Hub Genes and a Hormone-Mediated Defense Network Against Ralstonia solanacearum

## TL;DR

This study identifies key genes and a hormone-based defense network in tomatoes that help resist bacterial wilt, offering targets for breeding more resistant varieties.

## Contribution

The study reveals a hormone-mediated defense network and hub genes in tomato resistance to Ralstonia solanacearum using transcriptome and WGCNA analysis.

## Key findings

- Resistance involves hormone signaling, cell-wall reinforcement, and immune activation.
- Hub genes like ACO, ERF1, and RLK are strongly associated with defense responses.
- Ethylene and salicylic acid signaling are key in the resistance mechanism.

## Abstract

Tomato is a globally important crop that is severely threatened by bacterial wilt caused by Ralstonia solanacearum. The disease can lead to substantial yield losses. We conducted transcriptome analysis of the root, stem, and leaf tissues from resistant and susceptible tomato lines to elucidate the molecular basis of resistance. The results revealed a multi-layered defense system coordinated by key hub genes. These genes regulate cell-wall reinforcement, hormone signaling, and immune activation, collectively restricting pathogen colonization. The identified genes offer practical targets for marker-assisted selection and genome editing for the development of wilt-resistant tomato varieties. This strategy supports sustainable agriculture by reducing dependence on chemical pesticides.

Bacterial wilt caused by Ralstonia solanacearum is a major constraint on tomato (Solanum lycopersicum L.) production, yet the molecular basis of quantitative resistance remains poorly understood. In this study, comparative transcriptome profiling was performed on resistant (‘ZM3’) and susceptible (‘ZM86’) tomato inbred lines following pathogen inoculation in roots, stems, and leaves. Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were conducted to identify resistance-associated regulatory modules and hub genes. The results revealed distinct gene expression patterns between the two genotypes after infection. Several co-expression modules were significantly associated with resistance or susceptibility traits. Functional enrichment analysis showed that differentially expressed genes were mainly involved in plant hormone signal transduction, plant–pathogen interaction, phenylpropanoid biosynthesis, and cell wall modification. Genes related to ethylene and salicylic acid signaling were strongly induced following infection, whereas brassinosteroid-associated genes showed genotype-dependent expression patterns. Network analysis further identified several hub genes within defense-related modules, including ACO (Solyc04g007980), ERF1 (Solyc09g091950), MAPK9, receptor-like kinase RLK (Solyc07g006770), and a dirigent family gene (Solyc10g008900). Taken together, our results suggest that tomato resistance to Ralstonia solanacearum involves a coordinated defense network integrating hormone-mediated transcriptional regulation and structural reinforcement, and provides candidate genes for breeding bacterial wilt-resistant cultivars.