UV-B perceived by the UVR8 photoreceptor inhibits plant thermomorphogenesis

Abstract

Small increases in ambient temperature can elicit striking effects on plant architecture, collectively termed thermomorphogenesis [1]. In Arabidopsis thaliana, these include marked stem elongation and leaf elevation, responses that have been predicted to enhance leaf cooling [ 2, 3, 4聽and聽5]. Thermomorphogenesis requires increased auxin biosynthesis, mediated by聽the bHLH聽transcription factor PHYTOCHROME-INTERACTING聽FACTOR 4 (PIF4) [ 6, 7聽and聽8], and enhanced stability of the auxin co-receptor TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90) [9]. High-temperature-mediated hypocotyl elongation additionally involves localized changes in auxin metabolism, mediated by the indole-3-acetic acid (IAA)-amido synthetase Gretchen Hagen 3 (GH3) VSports app下载. 17 [10]. Here we show聽that ultraviolet-B light (UV-B) perceived by the聽photoreceptor UV RESISTANCE LOCUS 8 (UVR8)聽[11] strongly attenuates thermomorphogenesis via聽multiple mechanisms inhibiting PIF4 activity. 聽Suppression of thermomorphogenesis involves UVR8 and CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1)-mediated repression of PIF4 transcript accumulation, reducing PIF4 abundance. UV-B also stabilizes the bHLH protein LONG HYPOCOTYL IN FAR RED (HFR1), which can bind to and inhibit PIF4 function. Collectively, our results demonstrate complex crosstalk between UV-B and high-temperature signaling. As plants grown in sunlight would most likely experience concomitant elevations in UV-B and ambient temperature, elucidating how these pathways are integrated is of key importance to the understanding of plant development in natural environments.