Two signal molecules, salicylic acid (SA) and N-hydroxypipecolic acid (NHP), play critical roles in plant immunity. The biosynthetic genes of both compounds are positively regulated by master immune-regulating transcr...Two signal molecules, salicylic acid (SA) and N-hydroxypipecolic acid (NHP), play critical roles in plant immunity. The biosynthetic genes of both compounds are positively regulated by master immune-regulating transcription factors SARD1 and CBP60g. However, the relationship between the SA and NHP pathways is unclear. CALMODULIN-BINDING TRANSCRIPTION FACTOR 1 (CAMTA1), CAMTA2, and CAMTA3 are known redundant negative regulators of plant immunity, but the underlying mechanism also remains largely unknown. In this study, through chromatin immunoprecipitation and electrophoretic mobility shift assays, we uncovered that CBP60g is a direct target of CAMTA3, which also negatively regulates the expression of SARD1, presumably via an indirect effect. The autoimmunity of camta3-1 is suppressed by sard1 cbp60g double mutant as well as ald1 and fmo1, two single mutants defective in NHP biosynthesis. Interestingly, a suppressor screen conducted in the camta1/ 2/ 3 triple mutant background yielded various mutants blocking biosynthesis or signaling of either SA or NHP, leading to nearly complete suppression of the extreme autoimmunity of camta1/ 2/ 3, suggesting that the SA and NHP pathways can mutually amplify each other. Together, these results reveal that CAMTAs repress the biosynthesis of SA and NHP by modulating the expression of SARD1 and CBP60g, and that the SA and NHP pathways are coordinated to optimize plant immune response.展开更多
Summary Salicylic acid （SA） is an essential defence hormone in plants. Upon pathogen infection, induced biosynthesis of SA is mediated by Isochorismate synthase 1 （ICS1）, whose gene transcription is controlled mai...Summary Salicylic acid （SA） is an essential defence hormone in plants. Upon pathogen infection, induced biosynthesis of SA is mediated by Isochorismate synthase 1 （ICS1）, whose gene transcription is controlled mainly through two redundant transcription factors, SAR Deficient 1 （SARD0 and Calmodulin- binding protein 6o-like g （CBP60g）.展开更多
Arabidopsis SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1(SARD1)and CALMODULIN-BINDING PROTEIN 60g(CBP60g)are two master transcription factors that regulate many defense-related genes in plant immunity.They are required fo...Arabidopsis SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1(SARD1)and CALMODULIN-BINDING PROTEIN 60g(CBP60g)are two master transcription factors that regulate many defense-related genes in plant immunity.They are required for immunity downstream of the receptor-like protein SUPPRESSOR OF NPR1-1,CONSTITUTIVE 2(SNC2).Constitutive defense responses in the gain-of-function autoimmune snc2-1D mutant are modestly affected in either sard1 or cbp60g single mutants but completely suppressed in the sard1 cbp60g double mutant.Here we report that CBP60b,another member of the CBP60 family,also functions as a positive regulator of SNC2-mediated immunity.Loss-of-function mutations of CBP60b suppress the constitutive expression of SARD1 and enhanced disease resistance in cbp60g-1 snc2-1D,whereas overexpression of CBP60b leads to elevated SARD1 expression and constitutive defense responses.In addition,transient expression of CBP60b in Nicotiana benthamiana activates the expression of the pSARD1::luciferase reporter gene.Chromatin immunoprecipitation assays further showed that CBP60b is recruited to the promoter region of SARD1,suggesting that it directly regulates SARD1 expression.Interestingly,knocking out CBP60b in the wild-type background leads to ENHANCED DISEASE SUSCEPTIBILITY 1(EDS1)-dependent autoimmunity,suggesting that CBP60b is required for the expression of a guardee/decoy or a negative regulator of immunity mediated by receptors carrying an N-terminal Toll-interleukin-1 receptor-like domain.展开更多
文摘Two signal molecules, salicylic acid (SA) and N-hydroxypipecolic acid (NHP), play critical roles in plant immunity. The biosynthetic genes of both compounds are positively regulated by master immune-regulating transcription factors SARD1 and CBP60g. However, the relationship between the SA and NHP pathways is unclear. CALMODULIN-BINDING TRANSCRIPTION FACTOR 1 (CAMTA1), CAMTA2, and CAMTA3 are known redundant negative regulators of plant immunity, but the underlying mechanism also remains largely unknown. In this study, through chromatin immunoprecipitation and electrophoretic mobility shift assays, we uncovered that CBP60g is a direct target of CAMTA3, which also negatively regulates the expression of SARD1, presumably via an indirect effect. The autoimmunity of camta3-1 is suppressed by sard1 cbp60g double mutant as well as ald1 and fmo1, two single mutants defective in NHP biosynthesis. Interestingly, a suppressor screen conducted in the camta1/ 2/ 3 triple mutant background yielded various mutants blocking biosynthesis or signaling of either SA or NHP, leading to nearly complete suppression of the extreme autoimmunity of camta1/ 2/ 3, suggesting that the SA and NHP pathways can mutually amplify each other. Together, these results reveal that CAMTAs repress the biosynthesis of SA and NHP by modulating the expression of SARD1 and CBP60g, and that the SA and NHP pathways are coordinated to optimize plant immune response.
基金supported by grants from the Natural Sciences and Engineering Research Council of Canada(NSERC)Discovery programthe Dewar Cooper Memorial Fund from the University of British Columbia(UBC)+1 种基金partially supported by a 4YF scholarship from UBCpartially supported by a Chinese Scholarship Council(CSC)fellowship
文摘Summary Salicylic acid （SA） is an essential defence hormone in plants. Upon pathogen infection, induced biosynthesis of SA is mediated by Isochorismate synthase 1 （ICS1）, whose gene transcription is controlled mainly through two redundant transcription factors, SAR Deficient 1 （SARD0 and Calmodulin- binding protein 6o-like g （CBP60g）.
文摘Arabidopsis SYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1(SARD1)and CALMODULIN-BINDING PROTEIN 60g(CBP60g)are two master transcription factors that regulate many defense-related genes in plant immunity.They are required for immunity downstream of the receptor-like protein SUPPRESSOR OF NPR1-1,CONSTITUTIVE 2(SNC2).Constitutive defense responses in the gain-of-function autoimmune snc2-1D mutant are modestly affected in either sard1 or cbp60g single mutants but completely suppressed in the sard1 cbp60g double mutant.Here we report that CBP60b,another member of the CBP60 family,also functions as a positive regulator of SNC2-mediated immunity.Loss-of-function mutations of CBP60b suppress the constitutive expression of SARD1 and enhanced disease resistance in cbp60g-1 snc2-1D,whereas overexpression of CBP60b leads to elevated SARD1 expression and constitutive defense responses.In addition,transient expression of CBP60b in Nicotiana benthamiana activates the expression of the pSARD1::luciferase reporter gene.Chromatin immunoprecipitation assays further showed that CBP60b is recruited to the promoter region of SARD1,suggesting that it directly regulates SARD1 expression.Interestingly,knocking out CBP60b in the wild-type background leads to ENHANCED DISEASE SUSCEPTIBILITY 1(EDS1)-dependent autoimmunity,suggesting that CBP60b is required for the expression of a guardee/decoy or a negative regulator of immunity mediated by receptors carrying an N-terminal Toll-interleukin-1 receptor-like domain.
