UV RESISTANCE LOCUS8 mediates ultraviolet-B-induced stomatal closure in an ethylene-dependent manner

Abstract

Although the UV RESISTANCE LOCUS 8 (UVR8)-CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1)-ELONGATED HYPOCOTYL5 (HY5) signaling pathway, ethylene, hydrogen peroxide (H₂O₂), and nitric oxide (NO) all participate in ultraviolet-B (UV-B)-triggered stomatal closing, their interrelationship is not clear. Here, we found that UV-B-induced the expression of ethylene biosynthetic genes, production of ethylene, H₂O₂, and NO, and stomata closing were impaired in uvr8, cop1, and hy5 mutants. UV-B-induced NO production and stomata closing were also defective in mutants for ETHYLENE RESPONSE 1 (ETR1), ETHYLENE INSENSITIVE 2 (EIN2), and EIN3, but UV-B-triggered H₂O₂ generation was only inhibited in etr1. In either the absence or presence of UV-B, ethylene triggered H₂O₂ production but not NO generation and stomatal closure in cop1 and hy5, and stomata closing in cop1 and hy5 was induced by NO but not H₂O₂. Moreover, NO production and stomatal closure were constitutively caused by over-expression of COP1 or HY5 in ein2 and ein3, but not by over-expression of EIN2 or EIN3 in cop1 and hy5. Our data indicate that the UVR8-COP1-HY5 signaling module mediates UV-B-induced ethylene production, ethylene is then perceived by ETR1 to induce H₂O₂ synthesis. H₂O₂ induces NO generation and subsequent stomata closing via an EIN2, EIN3, COP1, and HY5-dependent pathway(s).

Keywords: Ethylene; Hydrogen peroxide; Nitric oxide; Stomatal movement; UV RESISTANCE LOCUS 8; Ultraviolet-B.