OXR2 integrates UV-B photomorphogenic signalling, DNA repair, cell cycle regulation, and phenolic compound accumulation in Arabidopsis thaliana.

Abstract

Ultraviolet-B radiation has a dual effect on plants, acting both as a developmental cue and a source of genetic stress. Plants must balance growth, DNA repair, cell division, and damage mitigation. Oxidation Resistance (OXR) proteins are evolutionarily conserved, TLDc-domain-containing mitochondrial proteins that link redox homeostasis to nuclear stress responses, which makes them strong candidates to coordinate the plant response to UV-B. This study highlights that the Arabidopsis protein AtOXR2 and its sunflower orthologue, HaOXR2, are critical for enhancing plant tolerance to UV-B radiation. Transgenic plants overexpressing AtOXR2 or HaOXR2 showed improved growth under UV-B radiation, with reduced inhibition of leaf, hypocotyl, and root development. Additionally, these plants exhibited reduced meristematic cell death and fewer cyclobutane pyrimidine dimers, a major form of UV-B-induced DNA damage. In vivo analysis using the PlaCCI reporter revealed that while wild-type plants arrest in the G2/M phase after UV-B, OXR2-overexpressing lines maintain a G1/S-enriched cell-cycle profile, suggesting reduced perception of UV-B damage. Furthermore, these plants showed elevated expression of genes associated with light signalling, DNA repair, and cell-cycle checkpoints, along with increased accumulation of protective phenolic and flavonoid compounds. Loss-of-function oxr2 mutants did not show reduced UV-B sensitivity, likely due to compensatory upregulation of compensatory mechanisms involving other OXR family members. Comparative transcriptomic analyses support a two-module model where OXR2 pre-activates the canonical UV-B damage response, thereby establishing OXR2 as an agronomic determinant of UV-B tolerance.