To compete with their neighbors for light and escape shaded environments, sun-loving plants have developed the shade-avoidance syndrome (SAS), a set of responses including alteration of plant architecture and initiation of early flowering and seed set. Previous studies on SAS mainly focused on dissecting molecular basis of hypocotyl elongation in seedlings under shade light; however, the molecular mechanisms underlying shade-accelerated flowering in adult plants remain unknown. In this study, we found that CONSTANS (CO) and PHYTOCHROME-INTERACTING FACTOR 7 (PIF7) have an additive effect on shade-induced flowering, but that LONG HYPOCOTYL IN FAR-RED1 (HFR1) represses early flowering by binding to CO and PIF7 and preventing the binding of CO to the promoter of FLOWERING LOCUS T (FT) and the binding of PIF7 to the promoter of pri-MIR156E/F. Under shade, de-phosphorylated PIF7 and accumulated CO, balanced by HFR1, upregulate the expression of FT, TSF, SOC1, and SPLs to accelerate flowering. Moreover, we found that the function of PIF7 in flowering time is independent of phyA. Collectively, these regulatory interactions establish a crucial link between the light signal and genetic network that regulates flowering transition under shade.

为了与邻居争夺光照和避光的阴影环境，爱好阳光的植物开发了避荫综合症（SAS），这是一组应对措施，包括改变植物结构以及启动早花期和结实期。以往对SAS的研究主要集中在解剖遮光下幼苗下胚轴伸长的分子基础上。然而，成年植物加速阴影开花的分子机制仍然未知。在这项研究中，我们发现CONSTANS（CO）和植物色素相互作用因子7（PIF7）对遮荫诱导的开花有累加作用，但FAR-RED1（HFR1）中的长羟基油菜碱通过与CO和PIF7结合而抑制早开花。并防止CO与FLOWERING LOCUS T（FT）以及PIF7与pri-MIR156E / F启动子的结合。下灯罩，去磷酸化和PIF7积累CO，通过HFR1平衡，上调的表达FT，TSF，SOC1和声压级加速开花。此外，我们发现PIF7在开花时间中的功能独立于phyA。总的来说，这些调节相互作用在光信号和调节阴影下开花过渡的遗传网络之间建立了至关重要的联系。