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

Abstract

Abstract: 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.