How plants protect themselves from ultraviolet-B radiation stress
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.
Working model of UV-B stress tolerance in Arabidopsis.
When plants are grown in white light (top, no UV-B conditions), UVR8 exists as an inactive homodimer. WRKY36 acts as a transcriptional repressor to repress HY5 transcription and COP1 promotes the ubiquitination and degradation of HY5 in the nucleus, thus repressing the transcription of UV-B-responsive genes. MYB13 binds to the promoters of flavonoid biosynthesis genes and promotes their expression; BR signaling activates BES1 to repress the transcription of PFG-MYBs controlling flavonoid biosynthesis.
When plants are grown in white light (top, no UV-B conditions), UVR8 exists as an inactive homodimer. WRKY36 acts as a transcriptional repressor to repress HY5 transcription and COP1 promotes the ubiquitination and degradation of HY5 in the nucleus, thus repressing the transcription of UV-B-responsive genes. MYB13 binds to the promoters of flavonoid biosynthesis genes and promotes their expression; BR signaling activates BES1 to repress the transcription of PFG-MYBs controlling flavonoid biosynthesis.
Under UV-B stress (bottom), UVR8 converts to monomers and accumulates in the nucleus. COP1 activity is repressed; thus the HY5 protein is stabilized and induces the transcription of UV-B responsive genes. UVR8 interacts with WRKY36 and inhibits WRKY36 DNA binding at the HY5 promoter. UVR8 enhances the affinity of MYB13 for the promoters of flavonoid biosynthesis genes. UV-B stress inhibits the expression of BES1 in a UVR8-independent manner to suppress the inhibition of PFG-MYBs; UV-B stress also activates ATR and MAPK pathways to increase UV-B stress tolerance.
The stabilization of HY5 by UV-B and visible light also induces RUPs and BICs transcription and thus promotes the feedback regulation of UVR8 and Cryptochrome photoreceptor activities. BBX24 is UV-B induced, and COP1 interacts with BBX24 and is required for BBX24 accumulation.
BBX24 also interacts with HY5 and antagonizes the function of HY5 in UV-B signaling.
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