Molecular Mechanisms of UVR8-Mediated Photomorphogenesis Derived from Revaluation of Action Spectra.

Abstract

Considering previously reported action spectra and molecular evidence, I propose a hypothetical model for UV RESISTANCE LOCUS8 (UVR8)-mediated photomorphogenesis. Upon UV-B irradiation, a UVR8 dimer dissociates and accumulates in the nucleus and photomorphogenesis begins following two pathways: one in which the UVR8 monomer binds to transcription factor(s) of gene(s) supporting hypocotyl growth to stop gene expression resulting in hypocotyl growth inhibition and the other in which the UVR8 monomer binds both with CONSTITUTIVELY PHOTOMORPHOGENIC1-SUPPRESSOR OF PHYA (COP1-SPA) to release HY5 (referred to as "stabilized") and WRKY DNA-BINDING PROTEIN 36 (WRKY36) on the ELONGATED HYPOCOTYL 5 (HY5) gene to release HY5 transcription, and both HY5 and another UV-B-activated UV-B sensor (denoted the Hyp sensor in this article) through a self-interacting factor (HIF) associates with the HY5 promoter to initiate HY5 transcription, leading to anthocyanin synthesis. These two pathways can be distinguished by action spectra in the UV-B region, with a single peak at 280nm and two peaks (or a broad peak near 280-300nm) for the former and the latter, respectively. Expanding the concept to cyanobacteria and other algae, I discuss the evolution of a UV-B sensor in green plants.