Ambient temperature induces the hypocotyl elongation of seedling,called as thermomorphogenesis.It has been reported that the bHLH transcriptional factor PIF7 acts as the critical component to modulate plant thermomorp...Ambient temperature induces the hypocotyl elongation of seedling,called as thermomorphogenesis.It has been reported that the bHLH transcriptional factor PIF7 acts as the critical component to modulate plant thermomorphogenesis,but the underlying mechanism remains elusive.The phytohormone abscisic acid(ABA)suppresses the hypocotyl elongation under high temperature(HT)stress.As the ABI5 binding protein,AFP2 acts as the negative factor to control ABA signaling.In this study,we first identified AFP2 as the interaction protein of PIF7 in vitro and in vivo.Phenotype analysis revealed that overexpressing AFP2 reduced the hypocotyl elongation,while loss-of-function afp2 mutant showed longer hypocotyl under HT.Consistently,overexpressing AFP2 impaired the transactivation effect of PIF7 on auxin biosynthesis related genes YUC8 and IAA19,which possibly resulted into the shorter hypocotyl in the transgenic line overexpressing AFP2 or co-overexpressing AFP2 and PIF7.Thus,these data suggest that AFP2 suppressed PIF7 activity to suppress hypocotyl elongation.Furthermore,we found that HT gradually induced the degradation of AFP2 that possibly released the inhibitory effect of AFP2 on PIF7,thus induced hypocotyl elongation under HT.Taken together,our result reveals the novel function of AFP2 in coordinating thermomorphogenesis through sophistically modulating PIF7 activity.展开更多
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...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.展开更多
基金funded by the National Natural Science Foundation of China(Grant No.31970289).
文摘Ambient temperature induces the hypocotyl elongation of seedling,called as thermomorphogenesis.It has been reported that the bHLH transcriptional factor PIF7 acts as the critical component to modulate plant thermomorphogenesis,but the underlying mechanism remains elusive.The phytohormone abscisic acid(ABA)suppresses the hypocotyl elongation under high temperature(HT)stress.As the ABI5 binding protein,AFP2 acts as the negative factor to control ABA signaling.In this study,we first identified AFP2 as the interaction protein of PIF7 in vitro and in vivo.Phenotype analysis revealed that overexpressing AFP2 reduced the hypocotyl elongation,while loss-of-function afp2 mutant showed longer hypocotyl under HT.Consistently,overexpressing AFP2 impaired the transactivation effect of PIF7 on auxin biosynthesis related genes YUC8 and IAA19,which possibly resulted into the shorter hypocotyl in the transgenic line overexpressing AFP2 or co-overexpressing AFP2 and PIF7.Thus,these data suggest that AFP2 suppressed PIF7 activity to suppress hypocotyl elongation.Furthermore,we found that HT gradually induced the degradation of AFP2 that possibly released the inhibitory effect of AFP2 on PIF7,thus induced hypocotyl elongation under HT.Taken together,our result reveals the novel function of AFP2 in coordinating thermomorphogenesis through sophistically modulating PIF7 activity.
基金This research was supported by the National Key R&D Program of China(2017YFA0503800).
文摘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.
