Identification of two key genes involved in flavonoid catabolism and their different roles in apple resistance to biotic stresses

New Phytol. 2024 May;242(3):1238-1256. doi: 10.1111/nph.19644. Epub 2024 Mar 1.

Abstract

Biosynthesis of flavonoid aglycones and glycosides is well established. However, key genes involved in their catabolism are poorly understood, even though the products of hydrolysis and oxidation play important roles in plant resistance to biotic stress. Here, we report on catabolism of dihydrochalcones (DHCs), the most abundant flavonoids in domesticated apple and wild Malus. Two key genes, BGLU13.1 and PPO05, were identified by activity-directed protein purification. BGLU13.1-A hydrolyzed phlorizin, (the most abundant DHC in domesticated apple) to produce phloretin which was then oxidized by PPO05. The process differed in some wild Malus, where trilobatin (a positional isomer of phlorizin) was mainly oxidized by PPO05. The effects of DHC catabolism on apple resistance to biotic stresses was investigated using transgenic plants. Either directly or indirectly, phlorizin hydrolysis affected resistance to the phytophagous pest two-spotted spider mite, while oxidation of trilobatin was involved in resistance to the biotrophic fungus Podosphaera leucotricha. DHC catabolism did not affect apple resistance to necrotrophic pathogens Valsa mali and Erwinia amylovara. These results suggest that different DHC catabolism pathways play different roles in apple resistance to biotic stresses. The role of DHC catabolism on apple resistance appeared closely related to the mode of invasion/damage used by pathogen/pest.

Keywords: Malus; dihydrochalcone; hydrolysis; oxidation; powdery mildew; two‐spotted mites.

MeSH terms

  • Flavonoids / metabolism
  • Malus* / metabolism
  • Phlorhizin / metabolism
  • Plant Diseases / genetics
  • Plant Diseases / microbiology
  • Polyphenols*
  • Stress, Physiological / genetics

Substances

  • trilobatin
  • Phlorhizin
  • Flavonoids
  • Polyphenols

Associated data

  • RefSeq/MK948096.1
  • RefSeq/U78872.1
  • RefSeq/EU048863.1
  • RefSeq/OR735558
  • RefSeq/OR735561