UV-B Perceived by the UVR8 Photoreceptor Inhibits Plant Thermomorphogenesis.
UV-B Perceived by the UVR8 Photoreceptor Inhibits Plant Thermomorphogenesis.
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DOI：
10.1016/j.cub.2016.11.004
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发表时间：
2017-01-09
期刊：
影响因子：
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通讯作者：
Franklin KA
中科院分区：
文献类型：
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作者：
Hayes S;Sharma A;Fraser DP;Trevisan M;Cragg-Barber CK;Tavridou E;Fankhauser C;Jenkins GI;Franklin KA
环境温度的小幅升高可以引起对植物构型的显著影响，统称为热形态发生。在拟南芥中，这些反应包括显著的茎伸长和叶片抬高，这些反应已被预测为增强叶片降温。热形态发生需要增加生长素的生物合成，由转录因子光敏色素相互作用因子4(PIF4)介导，并提高生长素共同受体TIR1的稳定性，涉及热休克蛋白90(HSP90)。高温介导的下胚轴伸长还涉及生长素代谢的局部变化，这种变化是由吲哚-3-乙酸(IAA)-氨基合成酶Gretchen Hagen3(GH3)介导的。在这里，我们展示了由光感受器UV抗性基因8(UVR8)感知的紫外线B光(UV-B)通过多种机制抑制PIF4活性来强烈减弱热形态发生。热形态发生的抑制涉及UVR8和结构性光形态发生蛋白1(COP1)介导的抑制PIF4转录积累，降低PIF4丰度。UV-B还可以稳定bHLH蛋白长下胚轴远红(HFR1)，该蛋白可以结合并抑制PIF4的功能。总而言之，我们的结果证明了UV-B和高温信号之间的复杂串扰。由于生长在阳光下的植物很可能会经历伴随而来的UV-B和环境温度的升高，因此阐明这些途径是如何整合的对于理解植物在自然环境中的发育至关重要。UVR8活性在高温下抑制生长素信号转导和茎伸长，UVR8与COP1作用抑制bHLH因子PIF4的转录丰度，UV-B介导的PIF4降解是温度依赖的UV-B稳定bHLH因子HFR1，它可以结合并抑制PIF4功能的Hayes等。结果表明，由UVR8光感受器感知的低剂量UV-B是高温诱导的茎伸长的有效抑制剂。这为植物在明亮的阳光下提供了一个重要的刹车机制，防止过度伸长生长，可能导致茎倒伏和根和叶生物量的严重减少。
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 that have been predicted to enhance leaf cooling. Thermomorphogenesis requires increased auxin biosynthesis, mediated by the bHLH transcription factor PHYTOCHROME-INTERACTING FACTOR 4 (PIF4), and enhanced stability of the auxin co-receptor TIR1, involving HEAT SHOCK PROTEIN 90 (HSP90). 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).17. Here we show that ultraviolet-B light (UV-B) perceived by the photoreceptor UV RESISTANCE LOCUS 8 (UVR8) strongly attenuates thermomorphogenesis via multiple mechanisms inhibiting PIF4 activity. 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. UVR8 activity inhibits auxin signaling and stem elongation at high temperature UVR8 acting with COP1 suppresses transcript abundance of the bHLH factor PIF4 UV-B-mediated degradation of PIF4 is temperature dependent UV-B stabilizes the bHLH factor HFR1, which can bind to and inhibit PIF4 function Hayes et al. show that low-dose UV-B, perceived by the UVR8 photoreceptor, is a potent inhibitor of high-temperature-induced stem elongation. This provides plants with an important braking mechanism in bright sunlight, preventing excessive elongation growth that could lead to stem lodging and critical reductions in root and leaf biomass.