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
Arabidopsis MORE AXILLARY GROWTH2 MAX2)is a key component in the strigolactone(SL)and karrikin(KAR)signaling pathways and regulates the degradation of SUPPRESSOR OF MAX21/SMAX1-like(SMAX1/SMXL)proteins,which are trans...Arabidopsis MORE AXILLARY GROWTH2 MAX2)is a key component in the strigolactone(SL)and karrikin(KAR)signaling pathways and regulates the degradation of SUPPRESSOR OF MAX21/SMAX1-like(SMAX1/SMXL)proteins,which are transcriptional co-repressors that regulate plant architecture,as well as abiotic and biotic stress responses.The max2 mutation reduces resistance against Pseudomonas syringae pv.tomato(Pst).To uncover the mechanism of MAX2-mediated resistance,we evaluated the resistance of various SL and KAR signaling pathway mutants.The resistance of SL-deficient mutants and of dwarf 14(d14)was similar to that of the wild-type,whereas the resistance of the karrikin insensitive 2(kai2)mutant was compromised,demonstrating that the KAR signaling pathway,not the SL signaling pathway,positively regulates the immune response.We measured the resistance of smaxl and smxl mutants,as well as the double,triple,and quadruple mutants with max2,which revealed that both the smax1 mutant and smx16/7/8 triple mutant rescue the low resistance phenotype of max2 and that SMAX1 accumulation diminishes resistance.The susceptibility of smax1D,containing a degradation-insensitive form of SMAX1,further confirmed the SMAX1 function in the resistance.The relationship between the accumulation of SMAX1/SMXLs and disease resistance suggested that the inhibitory activity of SMAX1 to resistance requires SMXL6/7/8.Moreover,the exogenous application of KAR2 enhanced resistance against Pst,but KAR-induced resistance depended on salicylic acid(SA)signaling.Inhibition of karrikin signaling delayed SA-mediated defense responses and inhibited pathogen-induced protein biosynthesis.Together,we propose that the MAX2-KAI2-SMAX1 complex regulates resistance with the assistance of SMXL6/7/8 and SA signaling and that SMAX1/SMXLs possibly form a multimeric complex with their target transcription factors to fine tune immune responses.展开更多
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 the Research Fund for the Doctoral Program of Higher Education of China(30123515110006)the National Natural Science Foundation of China(31371557 and 31571574)the China Postdoctoral Science Foundation(2014T70603 and 2013M540527)。
文摘Arabidopsis MORE AXILLARY GROWTH2 MAX2)is a key component in the strigolactone(SL)and karrikin(KAR)signaling pathways and regulates the degradation of SUPPRESSOR OF MAX21/SMAX1-like(SMAX1/SMXL)proteins,which are transcriptional co-repressors that regulate plant architecture,as well as abiotic and biotic stress responses.The max2 mutation reduces resistance against Pseudomonas syringae pv.tomato(Pst).To uncover the mechanism of MAX2-mediated resistance,we evaluated the resistance of various SL and KAR signaling pathway mutants.The resistance of SL-deficient mutants and of dwarf 14(d14)was similar to that of the wild-type,whereas the resistance of the karrikin insensitive 2(kai2)mutant was compromised,demonstrating that the KAR signaling pathway,not the SL signaling pathway,positively regulates the immune response.We measured the resistance of smaxl and smxl mutants,as well as the double,triple,and quadruple mutants with max2,which revealed that both the smax1 mutant and smx16/7/8 triple mutant rescue the low resistance phenotype of max2 and that SMAX1 accumulation diminishes resistance.The susceptibility of smax1D,containing a degradation-insensitive form of SMAX1,further confirmed the SMAX1 function in the resistance.The relationship between the accumulation of SMAX1/SMXLs and disease resistance suggested that the inhibitory activity of SMAX1 to resistance requires SMXL6/7/8.Moreover,the exogenous application of KAR2 enhanced resistance against Pst,but KAR-induced resistance depended on salicylic acid(SA)signaling.Inhibition of karrikin signaling delayed SA-mediated defense responses and inhibited pathogen-induced protein biosynthesis.Together,we propose that the MAX2-KAI2-SMAX1 complex regulates resistance with the assistance of SMXL6/7/8 and SA signaling and that SMAX1/SMXLs possibly form a multimeric complex with their target transcription factors to fine tune immune responses.
