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

Abstract

Plants respond to slight increases in ambient temperature by altering their architecture, a phenomenon collectively termed thermomorphogenesis. Thermomorphogenesis helps mitigate the damage caused by potentially harmful high-temperature conditions and is modulated by multiple environmental factors. Among these factors, ultraviolet-B (UV-B) light has been shown to strongly suppress this response. However, the molecular mechanisms by which UV-B light regulates thermomorphogenesis and the physiological roles of the UV-B-mediated suppression remain poorly understood. Here, we show that UV-B light inhibits thermomorphogenesis through the UV RESISTANCE LOCUS8 (UVR8)-CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1)-phytochrome B (phyB)/LONG HYPOCOTYL IN FAR RED 1 (HFR1) signaling pathway. We found that cop1 mutants maintain high levels of active phyB at high temperatures. Extensive genetic analyses revealed that the increased levels of phyB, HFR1, and CRY1 in cop1 mutants redundantly reduce both the level and the activity of PHYTOCHROME INTERACTING FACTOR4 (PIF4), a key positive regulator in thermomorphogenesis, thereby repressing this growth response. In addition, we found that UV-B light inactivates COP1 to enhance phyB stability and increase its photobody number. The UV-B-stabilized active phyB, in concert with HFR1, inhibits thermomorphogenesis by interfering with PIF4 activity. We further demonstrate that increased levels of active phyB enhance UV-B tolerance by promoting flavonoid biosynthesis and inhibiting thermomorphogenic growth. Taken together, our results elucidate that UV-B increases the levels of active phyB and HFR1 by inhibiting COP1 to suppress PIF4-mediated growth responses, which is crucial for plant tolerance to UV-B stress at high temperatures.