How plants protect themselves from ultraviolet-B radiation stress

Abstract

Abstract Ultraviolet-B (UV-B) radiation has a wavelength range of 280–315 nm. Plants perceive UV-B as an environmental signal and a potential abiotic stress factor that affects development and acclimation. UV-B regulates photomorphogenesis including hypocotyl elongation inhibition, cotyledon expansion, and flavonoid accumulation, but high intensity UV-B can also harm plants by damaging DNA, triggering accumulation of reactive oxygen species, and impairing photosynthesis. Plants have evolved “sunscreen” flavonoids that accumulate under UV-B stress to prevent or limit damage. The UV-B receptor UV RESISTANCE LOCUS 8 (UVR8) plays a critical role in promoting flavonoid biosynthesis to enhance UV-B stress tolerance. Recent studies have clarified several UVR8-mediated and UVR8-independent pathways that regulate UV-B stress tolerance. Here, we review these additions to our understanding of the molecular pathways involved in UV-B stress tolerance, highlighting the important roles of ELONGATED HYPOCOTYL 5, BRI1-EMS-SUPPRESSOR1, MYB DOMAIN PROTEIN 13, MAP KINASE PHOSPHATASE 1, and ATM- and RAD3-RELATED. We also summarize the known interactions with visible light receptors and the contribution of melatonin to UV-B stress responses. Finally, we update a working model of the UV-B stress tolerance pathway.