Tomato deploys defence and growth simultaneously to resist bacterial wilt disease

Plant Cell Environ. 2023 Oct;46(10):3040-3058. doi: 10.1111/pce.14456. Epub 2022 Oct 20.

Abstract

Plant disease limits crop production, and host genetic resistance is a major means of control. Plant pathogenic Ralstonia causes bacterial wilt disease and is best controlled with resistant varieties. Tomato wilt resistance is multigenic, yet the mechanisms of resistance remain largely unknown. We combined metaRNAseq analysis and functional experiments to identify core Ralstonia-responsive genes and the corresponding biological mechanisms in wilt-resistant and wilt-susceptible tomatoes. While trade-offs between growth and defence are common in plants, wilt-resistant plants activated both defence responses and growth processes. Measurements of innate immunity and growth, including reactive oxygen species production and root system growth, respectively, validated that resistant plants executed defence-related processes at the same time they increased root growth. In contrast, in wilt-susceptible plants roots senesced and root surface area declined following Ralstonia inoculation. Wilt-resistant plants repressed genes predicted to negatively regulate water stress tolerance, while susceptible plants repressed genes predicted to promote water stress tolerance. Our results suggest that wilt-resistant plants can simultaneously promote growth and defence by investing in resources that act in both processes. Infected susceptible plants activate defences, but fail to grow and so succumb to Ralstonia, likely because they cannot tolerate the water stress induced by vascular wilt.

Keywords: Hawaii7996; Ralstonia solanacearum; bacterial wilt; meta-transcriptomics; quantitative disease resistance; trade-off.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Dehydration
  • Genes, Plant
  • Plant Diseases* / microbiology
  • Solanum lycopersicum* / genetics
  • Solanum lycopersicum* / microbiology