Nitric oxide is a key part of the UV-B-induced photomorphogenesis in Arabidopsis

Ultraviolet-B (UV-B) radiation exerts a dual effect on plants. While high doses induce stress, lower doses act as a signal. The sensing of UV-B triggers a photomorphogenic response, causing changes like the hypocotyl shortening. This response is strongly regulated by the UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8). Although nitric oxide (NO) was proven to inhibit hypocotyl elongation in Arabidopsis thaliana , its role in UV-B-induced photomorphogenesis remains unclear. By using the NO probe DAF-FM DA, we found that UV-B radiation induced the accumulation of NO in the hypocotyl. This event is dependent on the presence of UVR8. Moreover, the NO donor S-nitrosoglutathione (GSNO), restored the WT phenotype when the Arabidopsis line lacking UVR8 was grown in the presence of UV-B. Also, we found that DELLA proteins were necessary for GSNO sensing in UV-B-induced photomorphogenesis. We showed that, through DELLAs, GSNO negatively controlled the levels of gibberellin (GA) bioprocessing-related genes. Therefore, a downregulation of GA signaling by NO is proposed. On the other hand, GSNO supplementation before UV-B treatment inhibited the induction of genes of the UVR8 signaling pathway: HY5 , CHS , and PHR1. This resulted in augmented DNA damage in short exposure to UV-B scenarios. Altogether, these results point to a complex regulation by NO of the UV-B-induced photomorphogenesis.

Automated summary

UV-B radiation has a dual effect on plants, acting as a signal at low doses and inducing stress at high doses. UV-B radiation induces the accumulation of NO in the hypocotyl, which is dependent on the presence of UVR8. The NO donor GSNO restores the WT phenotype in the absence of UVR8 and DELLAs are necessary for GSNO sensing in UV-B-induced photomorphogenesis.