Light is a key environmental factors affecting anthocyanin accumulation in plants. Ubiquitin E3 ligase COP1 has been proved to be a negative regulator involved in light-regulated plant development process, whereas the function and expression specificity of COP1 in anthocyanin biosynthesis in sweet cherry remains unclear. In the present study, we identified a COP1 in sweet cherry, named PacCOP1, it exhibited apparent different expression patterns in red-colored 'Hongdeng' and bi-colored 'Satonishiki', with increasing trend largely in 'Satonishiki', but decreasing trend in 'Hongdeng' after veraison, which was contrary to their variation tendency of anthocyanin content. While the expression abundance of anthocyanin biosynthesis related genes were largely increased after veraison, in accordance with anthocyanin content. Correlation analysis proved that the expression of PacCOP1 was negative correlated with the major genes on anthocyanin accumulation in 'Hongdeng' and 'Satonishiki' fruit, in especial PacDFR, PacANS, PacMYBA and PacbHLH33. Furthermore, over-expression of PacCOP1 in Arabidopsis displayed increased COP1 transcript level with negligible pigmentation and corresponding lower expression level of AtPAP1, AtDFR, AtLDOX, and AtUFGT. These results revealed the negative regular role of PacCOP1 in anthocyanin biosynthesis by repressing the PacMYBA transcription level, followed by down-regulating the structural genes expression abundance, eventually leading to attenuated anthocyanin accumulation in fruits.

中文翻译：

---

PacCOP1负调节甜樱桃（李属樱桃）中的花色苷生物合成。

光是影响植物中花色苷积累的关键环境因素。泛素E3连接酶COP1已被证明是负调节剂，参与光调节植物的发育过程，而COP1在甜樱桃花色苷生物合成中的功能和表达特异性仍不清楚。在本研究中，我们在甜樱桃中鉴定出一种名为PacCOP1的COP1，它在红色的“红灯”和双色的“ Satonishiki”中表现出明显不同的表达模式，其中“ Satonishiki”的趋势在很大程度上增加，而在“ Satonishiki”的趋势在下降检验后的“红灯”，与花青素含量的变化趋势相反。花色苷生物合成相关基因的表达丰度在检验后根据花色苷含量而大大增加。相关分析表明，PacCOP1的表达与“红灯”和“ Satonishiki”果实中的花色苷积累的主要基因呈负相关，特别是在PacDFR，PacANS，PacMYBA和PacbHLH33中。此外，PacCOP1在拟南芥中的过表达显示出COP1转录水平增加，色素沉着可忽略，并且相应的AtPAP1，AtDFR，AtLDOX和AtUFGT的表达水平较低。这些结果揭示了PacCOP1在花色苷生物合成中的负调控作用，其方式是抑制PacMYBA转录水平，然后下调结构基因的表达量，最终导致果实中花色苷的积累减弱。尤其是PacDFR，PacANS，PacMYBA和PacbHLH33中的“洪登”和“ Satonishiki”果实。此外，PacCOP1在拟南芥中的过表达显示出COP1转录水平增加，色素沉着可忽略，并且相应的AtPAP1，AtDFR，AtLDOX和AtUFGT的表达水平较低。这些结果揭示了PacCOP1在花色苷生物合成中的负调控作用，其方式是抑制PacMYBA转录水平，然后下调结构基因的表达量，最终导致果实中花色苷的积累减弱。尤其是PacDFR，PacANS，PacMYBA和PacbHLH33中的“洪登”和“ Satonishiki”果实。此外，PacCOP1在拟南芥中的过表达显示出COP1转录水平增加，色素沉着可忽略，并且相应的AtPAP1，AtDFR，AtLDOX和AtUFGT的表达水平较低。这些结果揭示了PacCOP1在花色苷生物合成中的负调控作用，其方式是抑制PacMYBA转录水平，然后下调结构基因的表达量，最终导致果实中花色苷的积累减弱。AtLDOX和AtUFGT。这些结果揭示了PacCOP1在花色苷生物合成中的负调控作用，其方式是抑制PacMYBA转录水平，然后下调结构基因的表达量，最终导致果实中花色苷的积累减弱。AtLDOX和AtUFGT。这些结果揭示了通过抑制PacMYBA转录水平，随后下调结构基因表达丰度，最终导致果实中花色苷积累减弱，PacCOP1在花色苷生物合成中的负调控作用。