Light signaling precisely controls photomorphogenic development in plants.PHYTOCHROME INTERACTING FACTOR 4 and 5(PIF4 and PIF5)play critical roles in the regulation of this developmental process.In this study,we repor...Light signaling precisely controls photomorphogenic development in plants.PHYTOCHROME INTERACTING FACTOR 4 and 5(PIF4 and PIF5)play critical roles in the regulation of this developmental process.In this study,we report CONSTITUTIVELY PHOTOMORPHOGENIC 1 SUPPRESSOR 6(CSU6)functions as a key regulator of light signaling.Loss of CSU6 function largely rescues the cop1-6 constitutively photomorphogenic phenotype.CSU6 promotes hypocotyl growth in the dark,but inhibits hypocotyl elongation in the light.CSU6 not only associates with the promoter regions of PIF4 and PIF5 to inhibit their expression in the morning,but also directly interacts with both PIF4 and PIF5 to repress their transcriptional activation activity.CSU6 negatively controls a group of PIF4-and PIF5-regulated gene expressions.Mutations in PIF4 and/or PIF5 are epistatic to the loss of CSU6,suggesting that CSU6 acts upstream of PIF4 and PIF5.Taken together,CSU6 promotes light-inhibited hypocotyl elongation by negatively regulating PIF4 and PIF5 transcription and biochemical activity.展开更多
Karrikins and strigolactones govern plant development and environmental responses through closely related signaling pathways.The transcriptional repressor proteins SUPPRESSOR OF MAX21(SMAX1),SMAX1-like2(SMXL2),and D53...Karrikins and strigolactones govern plant development and environmental responses through closely related signaling pathways.The transcriptional repressor proteins SUPPRESSOR OF MAX21(SMAX1),SMAX1-like2(SMXL2),and D53-like SMXLs mediate karrikin and strigolactone signaling by directly binding downstream genes or byinhibiting the activities of transcription factors.In this study,we characterized the non-transcriptional regulatory activities of SMXL proteins in Arabidopsis.We discovered that SMAX1 and SMXL2 with mutations in their ethylene-responsefactor-associated amphiphilic repression(EAR)motif had undetectable or weak transcriptional repression activities but still partially rescued the hypocotyl elongation defects and fully reversed the cotyledon epinasty defects of the smax1 smxl2 mutant.SMAX1 and SMXL2 directly interact with PHYTOCHROME INTERACTION FACTOR4(PIF4)and PIF5 to enhance their protein stability by interacting with phytochrome B(phyB)and suppressing the association of phyB with PIF4 and PIF5.The karrikin-responsive genes were then identified by treatment with GR24ent-ssa,GR24 analog showing karrikin activity.Interestingly,INDOLE-3-ACETIC ACID INDUCIBLE 29(IAA29)expression was repressed by GR24^(ent-5D)streatment in a PIF4-and PIF5-dependent and EARindependent manner,whereas KARRIKIN UPREGULATED F-BOX 1(KUF1)expression was induced in a PIF4-and PIF5-independent and EAR-dependent manner.Furthermore,the non-transcriptional regulatory activity of SMAX1,which is independent of the EAR motif,had a global effect on gene expression.Taken together,these results indicate that non-transcriptional regulatory activities of SMAX1 and SMXL2 mediate karrikin-regulated seedling response to red light.展开更多
Nitrogen(N)deficiency causes early leaf senescence,resulting in accelerated whole-plant maturation and severely reduced crop yield.However,the molecular mechanisms underlying N-deficiency-induced early leaf senescence...Nitrogen(N)deficiency causes early leaf senescence,resulting in accelerated whole-plant maturation and severely reduced crop yield.However,the molecular mechanisms underlying N-deficiency-induced early leaf senescence remain unclear,even in the model species Arabidopsis thaliana.In this study,we identified Growth,Development and Splicing 1(GDS1),a previously reported transcription factor,as a new regulator of nitrate(NO3)signaling by a yeast-one-hybrid screen using a NO3enhancer fragment from the promoter of NRT2.1.We showed that GDS1 promotes NO3 signaling,absorption and assimilation by affecting the expression of multiple NO3 regulatory genes,including Nitrate Regulatory Gene2(NRG2).Interestingly,we observedthat gds1mutants show early leaf senescence as well as reduced NO3-contentand Nuptake under N-deficient conditions.Further analyses indicated that GDS1 binds to the promoters of several senescence-related genes,including Phytochrome-lnteracting Transcription Factors 4 and 5(PIF4 and PIF5)and represses their expression.Interestingly,we found that N deficiency decreases GDS1 protein accumulation,and GDS1 could interact with Anaphase Promoting Complex Subunit 10(APC10).Genetic and biochemical experiments demonstrated that Anaphase Promoting Complex or Cyclosome(APC/C)promotes the ubiquitination and degradation of GDS1 under N deficiency,resulting in loss of PIF4 and PiF5 repression and consequent early leaf senescence.Furthermore,we discovered that overexpression of GDS1 could delay leaf senescence and improve seed yield and N-use efficiency(NUE)in Arabidopsis.In summary,our study uncovers a molecular framework illustrating a new mechanism underlying low-N-induced early leaf senescence and provides potential targets for genetic improvement of crop varieties with increased yield and NUE.展开更多
We investigated the diurnal dependence of the hypocotyl-growth responses to shade under sunlight-night cycles in Arabidopsis thaliana. Afternoon shade events promoted hypocotyl growth, while morning shade was ineffect...We investigated the diurnal dependence of the hypocotyl-growth responses to shade under sunlight-night cycles in Arabidopsis thaliana. Afternoon shade events promoted hypocotyl growth, while morning shade was ineffective. The Ihy-D, elf3, lux, pif4 pifS, tocl, and quadruple della mutants retained the response to afternoon shade and the lack of response to morning shade while the Ihyccal mutant responded to both morning and afternoon shade. ThephyB mutant, plants overexpressing the multidrug resistance-like membrane protein ABCB19, and the iaa17/axr3 loss-of-function mutant failed to respond to shade. Transient exposure of sunlight-grown seedlings to synthetic auxin in the afternoon caused a stronger promotion of hypocotyl growth than morning treatments. The promotion of hypocotyl growth by afternoon shade or afternoon auxin required light perceived by phytochrome A or cryptochromes during the previous hours of the photoperiod. Although the ELF4-ELF3-LUX complex, PIF4, PIF5, and DELLA are key players in the generation of diurnal hypocotyl-growth patterns, they exert a minor role in the control of the diurnal pattern of growth responses to shade. We conclude that the strong diurnal dependency of hypocotyl-growth responses to shade relates to the balance between the antagonistic actions of LHY-CCA1 and a light-derived signal.展开更多
In Arabidopsis seeds, germination is promoted only by phytochromes, principally phytochrome B （phyB） and phytochrome A （phyA）. Despite the abundant information concerning the molecular basis of phyB signaling down...In Arabidopsis seeds, germination is promoted only by phytochromes, principally phytochrome B （phyB） and phytochrome A （phyA）. Despite the abundant information concerning the molecular basis of phyB signaling downstream of PIF1/PIL5, the signaling network inducing germination by phyA is poorly known. Here, we describe the influence of phyA on the transcriptome of Arabidopsis seeds when germination is induced by a far-red （FR） pulse. The expression of 11% of the genome was significantly regulated by phyA. Most of the genes were up-regulated and the changes noted late （i.e. 5 h after a FR pulse）, whereas changes in down-regulated genes were more abundant earlier （i.e. 0.5 h after a FR pulse）. Auxin- and GA-associated elements were overrepresented in the genes that were modified by phyA. A significant number of genes whose expression was affected by phyA had not been previously reported to be dependent on PIL5. Among them, homozygotic mutant seeds of MYB66, a SAUR-like protein, PIN7, and GASA4 showed an impaired promo- tion of germination by phyA. Natural variation at the transcriptional level was found in early signaling and GA metabolic genes, but not in ABA metabolic and expansin genes between Columbia and Landsberg erecta accessions. Although phyA and phyB/PIL5 signaling pathways share some molecular components, our data suggest that phyA signaling is partially independent of PIL5 when germination is promoted by very low fluences of light.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos 32100199,31900210,and 31970258)the Peking-Tsinghua Center for Life Sciences(to X.W.D)+4 种基金the Southern University of Science and Technology(to X.W.D)the Jiangsu Natural Science Foundation for Distinguished Young Scholars(Grant No.BK20211525)the Jiangsu"Innovativeand Entrepreneurial Talent"program(to D.X.)the Nanjing Agricultural University(start-up funding to D.X.)the Jiangsu Collaborative Innovation Center for Modern Crop Production(to D.X.).
文摘Light signaling precisely controls photomorphogenic development in plants.PHYTOCHROME INTERACTING FACTOR 4 and 5(PIF4 and PIF5)play critical roles in the regulation of this developmental process.In this study,we report CONSTITUTIVELY PHOTOMORPHOGENIC 1 SUPPRESSOR 6(CSU6)functions as a key regulator of light signaling.Loss of CSU6 function largely rescues the cop1-6 constitutively photomorphogenic phenotype.CSU6 promotes hypocotyl growth in the dark,but inhibits hypocotyl elongation in the light.CSU6 not only associates with the promoter regions of PIF4 and PIF5 to inhibit their expression in the morning,but also directly interacts with both PIF4 and PIF5 to repress their transcriptional activation activity.CSU6 negatively controls a group of PIF4-and PIF5-regulated gene expressions.Mutations in PIF4 and/or PIF5 are epistatic to the loss of CSU6,suggesting that CSU6 acts upstream of PIF4 and PIF5.Taken together,CSU6 promotes light-inhibited hypocotyl elongation by negatively regulating PIF4 and PIF5 transcription and biochemical activity.
基金the National Natural Science Foundation of China(32170320,32122012,and 32270327)the Hebei Natural Science Foundation(C2022503003)the Youth Innovation Promotion Association of the Chinese Academy of Sciences(Y2023025).
文摘Karrikins and strigolactones govern plant development and environmental responses through closely related signaling pathways.The transcriptional repressor proteins SUPPRESSOR OF MAX21(SMAX1),SMAX1-like2(SMXL2),and D53-like SMXLs mediate karrikin and strigolactone signaling by directly binding downstream genes or byinhibiting the activities of transcription factors.In this study,we characterized the non-transcriptional regulatory activities of SMXL proteins in Arabidopsis.We discovered that SMAX1 and SMXL2 with mutations in their ethylene-responsefactor-associated amphiphilic repression(EAR)motif had undetectable or weak transcriptional repression activities but still partially rescued the hypocotyl elongation defects and fully reversed the cotyledon epinasty defects of the smax1 smxl2 mutant.SMAX1 and SMXL2 directly interact with PHYTOCHROME INTERACTION FACTOR4(PIF4)and PIF5 to enhance their protein stability by interacting with phytochrome B(phyB)and suppressing the association of phyB with PIF4 and PIF5.The karrikin-responsive genes were then identified by treatment with GR24ent-ssa,GR24 analog showing karrikin activity.Interestingly,INDOLE-3-ACETIC ACID INDUCIBLE 29(IAA29)expression was repressed by GR24^(ent-5D)streatment in a PIF4-and PIF5-dependent and EARindependent manner,whereas KARRIKIN UPREGULATED F-BOX 1(KUF1)expression was induced in a PIF4-and PIF5-independent and EAR-dependent manner.Furthermore,the non-transcriptional regulatory activity of SMAX1,which is independent of the EAR motif,had a global effect on gene expression.Taken together,these results indicate that non-transcriptional regulatory activities of SMAX1 and SMXL2 mediate karrikin-regulated seedling response to red light.
基金supported by grants from the National Natural Science Foundation of China(grant no.31970270)Y.W.,the Taishan Scholar Foundation to Y.W.,the National Research and Development Program of China(2021YFF1000401)+1 种基金Y.W.,and the National Natural Science Foundation of China(grant no.32200228)the Natural Science Foundation of Shandong Province(grant no.ZR2020QC028)to H.F.
文摘Nitrogen(N)deficiency causes early leaf senescence,resulting in accelerated whole-plant maturation and severely reduced crop yield.However,the molecular mechanisms underlying N-deficiency-induced early leaf senescence remain unclear,even in the model species Arabidopsis thaliana.In this study,we identified Growth,Development and Splicing 1(GDS1),a previously reported transcription factor,as a new regulator of nitrate(NO3)signaling by a yeast-one-hybrid screen using a NO3enhancer fragment from the promoter of NRT2.1.We showed that GDS1 promotes NO3 signaling,absorption and assimilation by affecting the expression of multiple NO3 regulatory genes,including Nitrate Regulatory Gene2(NRG2).Interestingly,we observedthat gds1mutants show early leaf senescence as well as reduced NO3-contentand Nuptake under N-deficient conditions.Further analyses indicated that GDS1 binds to the promoters of several senescence-related genes,including Phytochrome-lnteracting Transcription Factors 4 and 5(PIF4 and PIF5)and represses their expression.Interestingly,we found that N deficiency decreases GDS1 protein accumulation,and GDS1 could interact with Anaphase Promoting Complex Subunit 10(APC10).Genetic and biochemical experiments demonstrated that Anaphase Promoting Complex or Cyclosome(APC/C)promotes the ubiquitination and degradation of GDS1 under N deficiency,resulting in loss of PIF4 and PiF5 repression and consequent early leaf senescence.Furthermore,we discovered that overexpression of GDS1 could delay leaf senescence and improve seed yield and N-use efficiency(NUE)in Arabidopsis.In summary,our study uncovers a molecular framework illustrating a new mechanism underlying low-N-induced early leaf senescence and provides potential targets for genetic improvement of crop varieties with increased yield and NUE.
文摘We investigated the diurnal dependence of the hypocotyl-growth responses to shade under sunlight-night cycles in Arabidopsis thaliana. Afternoon shade events promoted hypocotyl growth, while morning shade was ineffective. The Ihy-D, elf3, lux, pif4 pifS, tocl, and quadruple della mutants retained the response to afternoon shade and the lack of response to morning shade while the Ihyccal mutant responded to both morning and afternoon shade. ThephyB mutant, plants overexpressing the multidrug resistance-like membrane protein ABCB19, and the iaa17/axr3 loss-of-function mutant failed to respond to shade. Transient exposure of sunlight-grown seedlings to synthetic auxin in the afternoon caused a stronger promotion of hypocotyl growth than morning treatments. The promotion of hypocotyl growth by afternoon shade or afternoon auxin required light perceived by phytochrome A or cryptochromes during the previous hours of the photoperiod. Although the ELF4-ELF3-LUX complex, PIF4, PIF5, and DELLA are key players in the generation of diurnal hypocotyl-growth patterns, they exert a minor role in the control of the diurnal pattern of growth responses to shade. We conclude that the strong diurnal dependency of hypocotyl-growth responses to shade relates to the balance between the antagonistic actions of LHY-CCA1 and a light-derived signal.
文摘In Arabidopsis seeds, germination is promoted only by phytochromes, principally phytochrome B （phyB） and phytochrome A （phyA）. Despite the abundant information concerning the molecular basis of phyB signaling downstream of PIF1/PIL5, the signaling network inducing germination by phyA is poorly known. Here, we describe the influence of phyA on the transcriptome of Arabidopsis seeds when germination is induced by a far-red （FR） pulse. The expression of 11% of the genome was significantly regulated by phyA. Most of the genes were up-regulated and the changes noted late （i.e. 5 h after a FR pulse）, whereas changes in down-regulated genes were more abundant earlier （i.e. 0.5 h after a FR pulse）. Auxin- and GA-associated elements were overrepresented in the genes that were modified by phyA. A significant number of genes whose expression was affected by phyA had not been previously reported to be dependent on PIL5. Among them, homozygotic mutant seeds of MYB66, a SAUR-like protein, PIN7, and GASA4 showed an impaired promo- tion of germination by phyA. Natural variation at the transcriptional level was found in early signaling and GA metabolic genes, but not in ABA metabolic and expansin genes between Columbia and Landsberg erecta accessions. Although phyA and phyB/PIL5 signaling pathways share some molecular components, our data suggest that phyA signaling is partially independent of PIL5 when germination is promoted by very low fluences of light.
