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Cross-Species Metabolomic Analyses In The Brassicaceae Reveals Common Responses To Ultraviolet-B Exposure.

Yue JingMutsumi WatanabeFayezeh AarabiAlisdair Robert FernieMonica BorghiTakayuki Tohge
Published in: Plant & cell physiology (2023)
Exposure to UV-B radiation, an intrinsic component of solar light, is detrimental to all living organisms as chromophore units of DNA, RNA, and proteins readily absorb high-energy photons. Indirect damage to the same molecules and lipids is mediated by elevated ROS levels, a side effect of exposure to UV-B stress. To protect themselves from UV-B radiation, plants produce phytochemical sunscreen, among which flavonoids have shown to be particularly effective. The core aglycone of flavonoid molecules is subjected to chemical decoration, such as glycosylation and acylation, further improving sunscreen properties. In particular, acylation, which adds a phenolic ring to flavonoid molecules, enhances the spectral absorption of UV-A and UV-B rays, providing this class of compounds exceptional shielding power. In this study, we comprehensively analyzed the responses to UV-B radiation in four Brassicaceae species, including Arabidopsis thaliana, Brassica napus, B. oleracea, and B. rapa. Our study revealed a complete reprogramming of the central metabolic pathway in response to UV-B radiation characterized by increased production of functional precursors of specialized metabolites with UV-B shielding properties, indicating a targeted effort of plant metabolism to provide increased protection. The analysis of specialized metabolites and transcripts revealed activation of the phenylpropanoid-acetate pathway leading to the production of specific classes of flavonoids and a cross-species increase of phenylacylated flavonoid glucosides with synapoyl-glycoside decorations. Interestingly, our analysis also revealed constitutive expression of acyltransferase genes of the class of serine carboxypeptidase-like (SCPL) protein and down-regulation in response to UV-B radiation, possibly independent from the ELONGATED HYPOCOTYL 5 (HY5) signaling pathway.
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