The Molecular Mechanism Regulating Flavonoid Production in Rhododendron chrysanthum Pall. Against UV-B Damage Is Mediated by RcTRP5

Elevated levels of reactive oxygen species (ROS) are caused by ultraviolet B radiation (UV-B) stress. In response, plants strengthen their cell membranes, impeding photosynthesis. Additionally, UV-B stress initiates oxidative stress within the antioxidant defense system and alters secondary metabolism, particularly by increasing the quantity of UV-absorbing compounds such as flavonoids. The v-myb avian myeloblastosis viral oncogene homolog (MYB) transcription factor (TF) may participate in a plant's response to UV-B damage through its regulation of flavonoid biosynthesis. In this study, we discovered that the photosynthetic activity of <i>Rhododendron chrysanthum</i> Pall. (<i>R. chrysanthum</i>) decreased when assessing parameters of chlorophyll (PSII) fluorescence parameters under UV-B stress. Concurrently, antioxidant system enzyme expression increased under UV-B exposure. A multi-omics data analysis revealed that acetylation at the K68 site of the RcTRP5 (telomeric repeat binding protein of <i>Rhododendron chrysanthum</i> Pall.) transcription factor was upregulated. This acetylation modification of RcTRP5 activates the antioxidant enzyme system, leading to elevated expression levels of peroxidase (POD), superoxide dismutase (SOD), and catalase (CAT). Upregulation is also observed at the K95 site of the chalcone isomerase (CHI) enzyme and the K178 site of the anthocyanidin synthase (ANS) enzyme. We hypothesize that <i>RcTRP5</i> influences acetylation modifications of CHI and ANS in flavonoid biosynthesis, thereby indirectly regulating flavonoid production. This study demonstrates that <i>R. chrysanthum</i> can be protected from UV-B stress by accumulating flavonoids. This could serve as a useful strategy for enhancing the plant's flavonoid content and provide a valuable reference for research on the metabolic regulation mechanisms of other secondary substances.