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Small increases in ambient temperature can elicit striking effects on plant architecture, collectively termed thermomorphogenesis . In Arabidopsis thaliana, these include marked stem elongation and leaf elevation; responses which have been predicted to enhance leaf cooling [2-5]. Thermomorphogenesis requires increased auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME INTERACTING FACTOR 4 (PIF4) [6-8] and enhanced stability of the auxin co-receptor, TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90) . High temperature-mediated hypocotyl elongation additionally involves localised changes in auxin metabolism, mediated by the indole-3-acetic acid (IAA)-amido synthetase Gretchen Hagen 3 (GH3).17 . Here, we show that ultraviolet-B light (UV-B) perceived by the photoreceptor UV RESISTANCE LOCUS8 (UVR8)  strongly attenuates thermomorphogenesis via multiple mechanisms inhibiting PIF4 activity. Suppression of thermomorphogenesis involves UVR8 and CONSTITUTIVELY PHOTOMORPHOGENIC1 (COP1)-mediated repression of PIF4 transcript accumulation, reducing PIF4 abundance. UV-B also stabilises 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 signalling. As plants grown in sunlight would likely experience concomitant elevations in UV-B and ambient temperature, elucidating how these pathways are integrated is of key importance to understanding of plant development in natural environments.
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