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To compete with their neighbors for light and escape shaded environments,sun-loving plants have devel-oped 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 molec-ular 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.