The photosynthetic acclimation of extremophile Eutrema salsugineum plants to red light (RL) (14 days, 150 µmol photons m^-2 s^-1, 660 nm) and the expression of the key photoreceptor apoprotein genes, transcription factors (TFs) and associated with phytochrome system MIR (microRNA) genes were studied. RL exposure induced an increase in the content of anthocyanin and total phenolic compounds and the level of Chls was decreased. The photosystem 2 electron transport rate and the number of open reaction centres (q_L) were not changed in RL plants, however, the levels of non-photochemical quenching (NPQ) and the regulated quantum yield of non-photochemical quenching Y(NPQ) were significantly higher in the RL plants. The rate of CO₂ uptake was decreased by almost 1.4-fold but the respiration and transpiration rates, as well as the stomatal conductance were not changed in the RL plants.

An increase in the expression of the photoreceptor apoprotein genes PHYA, PHYB and PHYC, the TF genes PIF4, PIF5 and miR395, miR408, miR165 and decreases in the levels of the transcripts of the TF gene HY5 and miR171, miR157, and miR827 were detected. The acclimation effect of photosynthetic apparatus to RL was accompanied by an increase of pigment content such as total phenolic compounds and carotenoids and it is due to the changes in the expression of the apoprotein phytochrome genes PHYA, PHYB, PHYC and phytochrome signalling TFs (PIF4, PIF5 and HY5) as well as MIR genes associated with phytochrome system.

极端微生物Eutrema salsugineum植物对红光 (RL)（14 天，150 µmol 光子 m ^-2 s ^-1，660 nm）的光合适应以及关键光感受器载脂蛋白基因、转录因子 (TF) 和与光敏色素相关的表达系统 MIR (microRNA) 基因进行了研究。RL 暴露导致花青素和总酚类化合物含量增加，而 Chls 水平降低。RL 植物的光系统 2 电子传输速率和开放反应中心的数量 (q _L ) 没有变化，但是，非光化学猝灭 (NPQ) 的水平和非光化学猝灭 Y(NPQ) 的调节量子产率在 RL 植物中显着更高。一氧化碳的比率₂吸收减少了近 1.4 倍，但 RL 植物的呼吸和蒸腾速率以及气孔导度没有改变。

检测到光感受器载脂蛋白基因PHYA、PHYB和PHYC、TF 基因PIF4、PIF5和 miR395、miR408、miR165 的表达增加，以及 TF 基因HY5和 miR171、miR157 和 miR827的转录水平降低. 光合器对 RL 的驯化效应伴随着总酚类化合物和类胡萝卜素等色素含量的增加，这是由于载脂蛋白光敏色素基因PHYA、PHYB、PHYC和光敏色素信号转导 TF（PIF4、 PIF5和HY5 ) 以及与光敏色素系统相关的 MIR 基因。