UV-B increases active phytochrome B to suppress thermomorphogenesis and enhance UV-B stress tolerance at high temperatures.

Plants respond to small increases in ambient temperature by changing their architecture, a response collectively termed thermomorphogenesis. Thermomorphogenesis is considered to attenuate the damage caused by potentially harmful high-temperature conditions, and multiple environmental factors can modulate this process. Among these factors, ultraviolet-B (UV-B) light has been shown to strongly suppress this response. However, the molecular mechanisms through which it regulates thermomorphogenesis and the physiological roles of the UV-B-mediated suppression of thermomorphogenesis remain poorly understood. Here, we show that UV-B inhibits thermomorphogenesis through the UVR8-COP1-phyB/HFR1 signaling module. We found that cop1 mutants maintain high levels of active phyB at high temperatures. Extensive genetic analyses revealed that the increased phyB, HFR1, and CRY1 in cop1 mutants redundantly reduce both the level and activity of a key positive regulator in thermomorphogenesis, PIF4, thereby repressing this growth response. Additionally, we found that UV-B light increases phyB stability and its photobody number through the inactivation of COP1. The UV-B-stabilized active phyB, together with HFR1, inhibits thermomorphogenesis by interfering with PIF4. We further show that the increased active phyB enhances UV-B tolerance by activating flavonoid biosynthesis and inhibiting thermomorphogenic growth. Taken together, our study demonstrates that UV-B increases the levels of active phyB and HFR1 by inhibiting COP1 to suppress PIF4-mediated growth responses, which is essential for plant tolerance to UV-B stress at high temperatures.