In response to far-red light(FR),FAR-RED ELONGATED HYPOCOTYL 1(FHY1)transports the photoactivated phytochrome A(phyA),the primary FR photoreceptor,into the nucleus,where it initiates FR signaling in plants.Light promo...In response to far-red light(FR),FAR-RED ELONGATED HYPOCOTYL 1(FHY1)transports the photoactivated phytochrome A(phyA),the primary FR photoreceptor,into the nucleus,where it initiates FR signaling in plants.Light promotes the 26S proteasome-mediated degradation of FHY1,which desensitizes FR signaling,but the underlying regulatory mechanism remains largely unknown.Here,we show that reversible SUMOylation of FHY1 tightly regulates this process.Lysine K32(K32)and K103 are major SUMOylation sites of FHY1.We found that FR exposure promotes the SUMOylation of FHY1,which accelerates its degradation.Furthermore,we discovered that ARABIDOPSIS SUMO PROTEASE 1(ASP1)interacts with FHY1 in the nucleus under FR and facilitates its deSUMOylation.FHY1 was strongly SUMOylated and its protein level was decreased in the asp1-1 loss-of-function mutant compared with that in the wild type under FR.Consistently,asp1-1 seedlings exhibited a decreased sensitivity to FR,suggesting that ASP1 plays an important role in the maintenance of proper FHY1 levels under FR.Genetic analysis further revealed that ASP1 regulates FR signaling through an FHY1-and phyA-dependent pathway.Interestingly,We found that continuous FR inhibits ASP1 accumulation,perhaps contributing to the desensitization of FR signaling.Taken together,these results indicate that FR-induced SUMOylation and ASP1-dependent deSUMOylation of FHY1 represent a key regulatory mechanism that fine-tunes FR signaling.展开更多
Photoreceptors of the phytochrome family control a multitude of responses in plants.Phytochrome A(phyA)is essential for far-red light perception,which is important for germination and seedling establishment in strong ...Photoreceptors of the phytochrome family control a multitude of responses in plants.Phytochrome A(phyA)is essential for far-red light perception,which is important for germination and seedling establishment in strong canopy shade.Translocation of phyA from the cytosol into nucleus is a key step in farred light signaling and requires FAR-RED ELONGATED HYPOCOTYL 1(FHY1)and FHY1-LIKE(FHL).FHY1/FHL bind to phyA downstream signaling components.Therefore,it has been suggested that FHY1/FHL also have a function in assembling phyA transcription factor complexes in the nucleus.Yet,in this study,we show that constitutively nuclear-localized phyA is active in the absence of FHY1 and FHL.Furthermore,an artificial FHY1,consisting of an SV40 NLS,a phyA binding site,and a YFP tag as spacer between them,complements the fhy1-3 fhl-1 double mutant.These findings show that FHY1 and FHL are not required for phyA downstream signaling in the nucleus.However,we found that lines expressing phyA-NLS-YFP are hypersensitive to red and far-red light and that slightly increased levels of constitutively nuclear-localized phyA result in photomorphogenic development in the dark.Thus,restricting phyA to the cytosol and inducing nuclear transport in light by interaction with FHY1/FHL might be important to suppress photomorphogenesis in the dark.展开更多
In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental swit...In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental switch are not well understood.Here,we show that a pair of Arabidopsis transcription factors essential for phytochrome A signaling,FAR-RED ELONGATED HYPOCOTYL3(FHY3)and FAR-RED IMPAIRED RESPONSE1(FAR1),regulate flowering time by integrating environmental light signals with the miR156-SPL module-mediated aging pathway.We found that FHY3 and FAR1 directly interact with three flowering-promoting SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE(SPL)transcription factors,SPL3,SPL4,and SPL5,and inhibit their binding to the promoters of several key flowering regulatory genes,including FRUITFUL(FUL),LEAFY(LFY),APETALA1(AP1),and MIR172C,thus downregulating their transcript levels and delaying flowering.Under simulated shade conditions,levels of SPL3/4/5 proteins increase,whereas levels of FHY3 and FAR1 proteins decline,thus releasing SPL3/4/5 from FHY3/FAR1 inhibition to allow activation of FUL,LFY,AP1,and MIR172C and,consequently,early flowering.Taken together,these results unravel a novel mechanism whereby plants regulate flowering time by integrating environmental cues(such as light conditions)and an internal developmental program(the miR156-SPL module-mediated aging pathway).展开更多
基金This work was supported by the National Natural Science Foundation of China(grant nos.31670186 and 31870238)the Chinese Academy of Sciences(ZDRW-ZS-2019-2-0101,KFJ-STS-ZDTP-076-1,and The Innovative Academy of Seed Design).
文摘In response to far-red light(FR),FAR-RED ELONGATED HYPOCOTYL 1(FHY1)transports the photoactivated phytochrome A(phyA),the primary FR photoreceptor,into the nucleus,where it initiates FR signaling in plants.Light promotes the 26S proteasome-mediated degradation of FHY1,which desensitizes FR signaling,but the underlying regulatory mechanism remains largely unknown.Here,we show that reversible SUMOylation of FHY1 tightly regulates this process.Lysine K32(K32)and K103 are major SUMOylation sites of FHY1.We found that FR exposure promotes the SUMOylation of FHY1,which accelerates its degradation.Furthermore,we discovered that ARABIDOPSIS SUMO PROTEASE 1(ASP1)interacts with FHY1 in the nucleus under FR and facilitates its deSUMOylation.FHY1 was strongly SUMOylated and its protein level was decreased in the asp1-1 loss-of-function mutant compared with that in the wild type under FR.Consistently,asp1-1 seedlings exhibited a decreased sensitivity to FR,suggesting that ASP1 plays an important role in the maintenance of proper FHY1 levels under FR.Genetic analysis further revealed that ASP1 regulates FR signaling through an FHY1-and phyA-dependent pathway.Interestingly,We found that continuous FR inhibits ASP1 accumulation,perhaps contributing to the desensitization of FR signaling.Taken together,these results indicate that FR-induced SUMOylation and ASP1-dependent deSUMOylation of FHY1 represent a key regulatory mechanism that fine-tunes FR signaling.
基金This study was supported by the German Research Foundation(DFG)under Germany’s Excellence Strategy(BIOSS-EXC-294,CIBSS-EXC-2189-Project ID 390939984)by grants from the DFG(DFG HI 1369/4-1 and HI 1369/5-1)+2 种基金the Human Frontier Science Program Organization(HFSP research grant RGP0025/2013)to A.H.C.K.was supported by the Ministry of Science,Research and the Arts Baden-WuerttembergThe article processing charge was funded by the German Research Foundation(DFG)and the Albert Ludwigs University Freiburg in the funding programme Open Access Publishing.
文摘Photoreceptors of the phytochrome family control a multitude of responses in plants.Phytochrome A(phyA)is essential for far-red light perception,which is important for germination and seedling establishment in strong canopy shade.Translocation of phyA from the cytosol into nucleus is a key step in farred light signaling and requires FAR-RED ELONGATED HYPOCOTYL 1(FHY1)and FHY1-LIKE(FHL).FHY1/FHL bind to phyA downstream signaling components.Therefore,it has been suggested that FHY1/FHL also have a function in assembling phyA transcription factor complexes in the nucleus.Yet,in this study,we show that constitutively nuclear-localized phyA is active in the absence of FHY1 and FHL.Furthermore,an artificial FHY1,consisting of an SV40 NLS,a phyA binding site,and a YFP tag as spacer between them,complements the fhy1-3 fhl-1 double mutant.These findings show that FHY1 and FHL are not required for phyA downstream signaling in the nucleus.However,we found that lines expressing phyA-NLS-YFP are hypersensitive to red and far-red light and that slightly increased levels of constitutively nuclear-localized phyA result in photomorphogenic development in the dark.Thus,restricting phyA to the cytosol and inducing nuclear transport in light by interaction with FHY1/FHL might be important to suppress photomorphogenesis in the dark.
基金supported by grants from National Natural Science Foundation of China(31770210 and 31570191)National Key Research and D evelopm ent Program of China(2016YFD0100303).
文摘In response to competition for light from their neighbors,shade-intolerant plants flower precociously to ensure reproductive success and survival.However,the molecular mechanisms underlying this key developmental switch are not well understood.Here,we show that a pair of Arabidopsis transcription factors essential for phytochrome A signaling,FAR-RED ELONGATED HYPOCOTYL3(FHY3)and FAR-RED IMPAIRED RESPONSE1(FAR1),regulate flowering time by integrating environmental light signals with the miR156-SPL module-mediated aging pathway.We found that FHY3 and FAR1 directly interact with three flowering-promoting SQUAMOSA-PROMOTER BINDING PROTEIN-LIKE(SPL)transcription factors,SPL3,SPL4,and SPL5,and inhibit their binding to the promoters of several key flowering regulatory genes,including FRUITFUL(FUL),LEAFY(LFY),APETALA1(AP1),and MIR172C,thus downregulating their transcript levels and delaying flowering.Under simulated shade conditions,levels of SPL3/4/5 proteins increase,whereas levels of FHY3 and FAR1 proteins decline,thus releasing SPL3/4/5 from FHY3/FAR1 inhibition to allow activation of FUL,LFY,AP1,and MIR172C and,consequently,early flowering.Taken together,these results unravel a novel mechanism whereby plants regulate flowering time by integrating environmental cues(such as light conditions)and an internal developmental program(the miR156-SPL module-mediated aging pathway).
