In dense canopy, a reduction in red to far‐red (R/FR) light ratio triggers shade avoidance responses (SARs) in Arabidopsis thaliana, a shade avoiding plant. Two red/far‐red (R/FR) light photoreceptors, PHYB and PHYA, were reported to be key negative regulators of the SARs. PHYB represses the SARs under normal light conditions; however, the role of PHYA in the SARs remains elusive. We set up two shade conditions: Shade and strong Shade (s‐Shade) with different R/FR ratios (0.7 and 0.1), which allowed us to observe phenotypes dominated by PHYB‐ and PHYA‐mediated pathway, respectively. By comparing the hypocotyl growth under these two conditions with time, we found PHYA was predominantly activated in the s‐Shade after prolonged shade treatment. We further showed that under s‐Shade, PHYA inhibits hypocotyl elongation partially through repressing the brassinosteroid (BR) pathway. COP1 and PIF4,5 act downstream of PHYA. After prolonged shade treatment, the nuclear localization of COP1 was reduced, while the PIF4 protein level was much lower in the s‐Shade than that in Shade. Both changes occurred in a PHYA‐dependent manner. We propose that under deep canopy, the R/FR ratio is extremely low, which promotes the nuclear accumulation of PHYA. Activated PHYA reduces COP1 nuclear speckle, which may lead to changes of downstream targets, such as PIF4,5 and HY5. Together, these proteins regulate the BR pathway through modulating BES1/BZR1 and the expression of BR biosynthesis and BR target genes.

中文翻译：

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植物色素A通过抑制拟南芥中的油菜素类固醇途径，在强阴影下抑制避光反应。

在茂密的树冠中，红光到远红光（R / FR）的比率降低会触发拟南芥中的避光响应（SAR），避阴植物。据报道，两个红/远红（R / FR）光感受器PHYB和PHYA是SAR的关键负调节剂。PHYB可在正常光线条件下抑制SAR；但是，PHYA在SAR中的作用仍然难以捉摸。我们设置了两个阴影条件：具有不同R / FR比（0.7和0.1）的阴影和强阴影（s-Shade），这使我们能够分别观察到以PHYB和PHYA介导的途径为主的表型。通过比较这两种条件下下胚轴的生长与时间​​的关系，我们发现PHYA在长时间的遮光处理后主要在s-Shade中被激活。我们进一步表明，在s-Shade下，PHYA通过抑制油菜素类固醇（BR）途径部分抑制下胚轴伸长。COP1和PIF4,5在PHYA的下游起作用。经过长时间的遮光处理 COP1的核定位降低了，而s-Shade中的PIF4蛋白水平要比Shade中的低得多。两种更改均以PHYA相关的方式发生。我们建议在深层树冠下，R / FR比极低，这会促进PHYA的核积累。活化的PHYA可降低COP1核斑点，这可能导致下游靶标（例如PIF4,5和HY5）发生变化。这些蛋白质一起通过调节BES1 / BZR1以及BR生物合成和BR靶基因的表达来调节BR通路。这可能会导致下游目标（例如PIF4,5和HY5）的变化。这些蛋白质一起通过调节BES1 / BZR1以及BR生物合成和BR靶基因的表达来调节BR通路。这可能会导致下游目标（例如PIF4,5和HY5）的变化。这些蛋白质共同通过调节BES1 / BZR1以及BR生物合成和BR目标基因的表达来调节BR途径。