The blue light receptor CRY1 interacts with GID1 and DELLA proteins to repress GA signaling during photomorphogenesis in Arabidopsis

Light is a critical environmental cue that regulates a variety of diverse plant developmental processes.Cryptochrome 1(CRY1)is the major photoreceptor that mediates blue light-dependent photomorphogenic responses such as the inhibition of hypocotyl elongation.Gibberellin(GA)participates in the repression of photomorphogenesis and promotes hypocotyl elongation.However,the antagonistic interaction between blue light and GA is not well understood.Here,we report that blue light represses GA-induced degradation of the DELLA proteins(DELLAs),which are key negative regulators in the GA signaling pathway,via CRY1,thereby inhibiting the GA response during hypocotyl elongation.Both in vitro and in vivo biochemical analyses demonstrated that CRY1 physically interacts with GA receptors-GA-INSENSITIVE DWARF 1 proteins(GID1s)-and DELLAs in a blue light-dependent manner.Furthermore,we showed that CRY1 inhibits the association between GID1s and DELLAs.Genetically,CRY1 antagonizes the function of GID1s to repress the expression of cell elongation-related genes and thus hypocotyl elongation.Taken together,our findings demonstrate that CRY1 coordinates blue light and GA signali ng for plant photomorphogenesis by stabilizing DELLAs through the binding and in activation of GID1s,providing new in sights into the mechanism by which blue light antagonizes the function of GA in photomorphogenesis.

FKF1 F-box protein promotes flowering in part by negatively regulating DELLA protein stability under long-day photoperiod in Arabidopsis^FA

FLAVIN-BINDING KELCH REPEAT F-BOX 1(FKF1)encodes an F-box protein that regulates photoperiod flowering in Arabidopsis under long-day conditions(LDs).Gibberellin(GA)is also important for regulating flowering under LDs.However,how FKF1 and the GA pathway work in concert in regulating flowering is not fully understood.Here,we showed that the mutation of FKF1 could cause accumulation of DELLA proteins,which are crucial repressors in GA signaling pathway,thereby reducing plant sensitivity to GA in flowering.Both in vitro and in vivo biochemical analyses demonstrated that FKF1 directly interacted with DELLA proteins.Furthermore,we showed that FKF1 promoted ubiquitination and degradation of DELLA proteins.Analysis of genetic data revealed that FKF1 acted partially through DELLAs to regulate flowering under LDs.In addition,DELLAs exerted a negative feedback on FKF1 expression.Collectively,these findings demonstrate that FKF1 promotes flowering partially by negatively regulating DELLA protein stability under LDs,and suggesting a potential mechanism linking the FKF1 to the GA signaling DELLA proteins.

Construction and Validation of a Dual-Transgene Vector System for Stable Transformation in Plants

In this study,we constructed dual-transgene vectors（pDT1,pDT7,and pDT7G） that simultaneously co-expressed two genes in plants.ACTIN2 and UBQ10 promoters were used to control the expression of these two genes.The 4×Myc.3×HA,and 3×Flag reporter genes allowed for the convenient identification of a tunable co-expression system in plants,whereas the dexamethasone（Dex） inducible reporter gene C-terminus of the glucocorticoid receptor（cGR） provided Dex-dependent translocation of the fusion gene between the nucleus and cytoplasm.The function of pDT vectors was validated using four pairwise genes in Nicotiana benthamiana or Anihidopsis thaliana.The co-expression efficiency of two genes from the pDT1 and pDT7 G vectors was 35%and 42%,respectively,which ensured the generation of sufficient transgenic materials.These pDT vectors are simple,reliable,efficient,and time-saving tools for the co-expression of two genes through a single transformation event and can be used in the study of protein-protein interactions or multi-component complexes.