Jasmonates （JAs） are plant hormones with essential roles in plant defense and development. The basic- helix-loop-helix （bHLH） transcription factor （TF） MYC2 has recently emerged as a master regulator of most asp...Jasmonates （JAs） are plant hormones with essential roles in plant defense and development. The basic- helix-loop-helix （bHLH） transcription factor （TF） MYC2 has recently emerged as a master regulator of most aspects of the jasmonate （JA） signaling pathway in Arabidopsis. MYC2 coordinates JA-mediated defense responses by antagonistically regulating two different branches of the JA signaling pathway that determine resistance to pests and pathogens, respectively. MYC2 is required for induced systemic resistance （ISR） triggered by beneficial soil microbes while MYC2 function is targeted by pathogens during effector-mediated suppression of innate immunity in roots. Another notable function of MYC2 is the regulation of crosstalk between the signaling pathways of JA and those of other phytohormones such as abscisic acid （ABA）, salicylic acid （SA）, gibberellins （GAs）, and auxin （IAA）. MYC2 also regulates interactions between JA signaling and light, phytochrome signaling, and the circadian clock, MYC2 is involved in JA-regulated plant development, lateral and adventitious root formation, flowering time, and shade avoidance syndrome. Related bHLH TFs MYC3 and MYC4 also regulate both overlapping and distinct MYC2-regulated functions in Arabidopsis while MYC2 orthologs act as ＇master switches＇ that regulate JA-mediated biosynthesis of secondary metabolites. Here, we briefly review recent studies that revealed mechanistic new insights into the mode of action of this versatile TF.展开更多
There is increasing evidence that pathogens do not only elicit direct defense responses, but also cause pronounced changes in primary carbohydrate metabolism. Cell-wall-bound invertases belong to the key regulators of...There is increasing evidence that pathogens do not only elicit direct defense responses, but also cause pronounced changes in primary carbohydrate metabolism. Cell-wall-bound invertases belong to the key regulators of carbohydrate partitioning and source-sink relations. Whereas studies have focused so far only on the transcriptional induction of invertase genes in response to pathogen infection, the role of post-translational regulation of invertase activity has been neglected and was the focus of the present study. Expression analyses revealed that the high mRNA level of one out of three proteinaceous invertase inhibitors in source leaves of Arabidopsis thaliana is strongly repressed upon infection by a virulent strain of Pseudomonas syringae pv. tomato DC3000. This repression is paralleled by a decrease in invertase inhibitor activity. The physiological role of this regulatory mechanism is revealed by the finding that in situ invertase activity was detectable only upon infection by P. syringae. In contrast, a high invertase activity could be measured in vitro in crude and cell wall extracts prepared from both infected and non-infected leaves. The discrepancy between the in situ and in vitro invertase activity of control leaves and the high in situ invertase activity in infected leaves can be explained by the pathogen-dependent repression of invertase inhibitor expression and a concomitant reduction in invertase inhibitor activity. The functional importance of the release of invertase from post-translational inhibition for the defense response was substantiated by the application of the competitive chemical invertase inhibitor acarbose. Posttranslational inhibition of extracellular invertase activity by infiltration of acarbose in leaves was shown to increase the susceptibility to P. syringae. The impact of invertase inhibition on spatial and temporal dynamics of the repression of photosynthesis and promotion of bacterial growth during pathogen infection supports a role for extracellular invertase in plant defen展开更多
The Arabidopsis accelerated cell death 6-1 （acd6-1） mutant shows constitutive defense, cell death, and ex- treme dwarf phenotypes. In a screen for acd6-1 suppressors, we identified a mutant that was disrupted by a T...The Arabidopsis accelerated cell death 6-1 （acd6-1） mutant shows constitutive defense, cell death, and ex- treme dwarf phenotypes. In a screen for acd6-1 suppressors, we identified a mutant that was disrupted by a T-DNA in the PHOSPHATE TRANSPORTER 4;1 （PHT4;1） gene. The suppressor mutant pht4;1-1 is dominant, expresses truncated PHT4;1 transcripts, and is more susceptible to virulent Pseudomonas syringae strains but not to several avirulent strains. Treat- ment with a salicylic acid （SA） agonist induced a similar level of resistance in Col-0 and pht4;1-1, suggesting that PHT4;1 acts upstream of the SA pathway. Genetic analysis further indicates that PHT4,1 contributes to SID2-dependent and -in- dependent pathways. Transgenic expression of the DNA fragment containing the PHT4;1-1 region or the full-length PHT4;1 gene in wild-type conferred enhanced susceptibility to Pseudomonas infection. Interestingly, expression of PHT4;1 is reg- ulated by the circadian clock. Together, these data suggest that the phosphate transporter PHT4;1 is critical for basal defense and also implicate a potential role of the circadian clock in regulating innate immunity of Arabidopsis.展开更多
In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disea...In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.展开更多
The Pto protein kinase from Solanum pimpinellifolium interacts with Pseudomonas syringae effectors AvrPto or AvrPtoB to activate effector-triggered immunity. The previously solved crystal structures of the AvrPto-Pto ...The Pto protein kinase from Solanum pimpinellifolium interacts with Pseudomonas syringae effectors AvrPto or AvrPtoB to activate effector-triggered immunity. The previously solved crystal structures of the AvrPto-Pto and AvrPtoB-Pto complexes revealed that Pro binds each effector through both a shared and a unique interface. Hera we use natural variation in wild species of tomato to further investigate Pto recognition of these two effectors. One species, Solanum chmielewskU, was found to have many accessions that recognize only AvrPtoB. The Pto ortholog from one of these accessions was responsible for recognition of AvrPtoB and it differed from Solanum pimpinellifolium Pto by only 14 amino acids, including two in the AvrPto-specific interface, glutamate-49/glycine-51. Converting these two residues to those in Pro （histidine-49/valine-51） did not restore recognition of AvrPto. Subsequent experiments revealed that a single substitution of a histidine-to-aspartate at position 193 in Pto, which is not near the AvrPto- specific interface, was sufficient for conferring recognRion of AvrPto in plant cells. The reciprocal substi- tution of aspartate-to-histidine-193 in Pto abolished AvrPto recognition, confirming the importance of this residue. Our results reveal new aspects about effector recognition by Pto and demonstrate the value of using natural variation to understand the interaction between resistance proteins and pathogen effectors.展开更多
Tryptophan-derived, indolic metabolites possess diverse functions in Arabidopsis innate immunity to microbial pathogen infection. Hers, we investigate the functional role and regulatory characteristics of indolic meta...Tryptophan-derived, indolic metabolites possess diverse functions in Arabidopsis innate immunity to microbial pathogen infection. Hers, we investigate the functional role and regulatory characteristics of indolic metabolism in Arabidopsis systemic acquired resistance （SAR） triggered by the bacterial pathogen Pseudomonas syringae. Indolic metabolism is broadly activated in both P. syringae-inoculated and distant, non-inoculated leaves. At inoculation sites, camalexin, indol-3-ylmethylamine （13A）, and indole-3-carboxylic acid （ICA） are the major accumulating compounds. Camalexin accumulation is positively affected by MYB122, and the cytochrome P450 genes CYP81F1 and CYP81F2. Local 13A production, by contrast, occurs via indole glucosinolate breakdown by PEN2- dependent and independent pathways. Moreover, exogenous application of the defense hormone salicylic acid stimulates 13A generation at the expense of its precursor indol-3-ylmethylglucosinolate （13M）, and the SAR regulator pipecolic acid primes plants for enhanced P. syringae-induced activation of distinct branches of indolic metabolism. In uninfected systemic tissue, the metabolic response is more specific and associated with enhanced levels of the indolics 13A, ICA, and indole-3-carbaldehyde （ICC）. Systemic indole accumulation fully depends on functional CYP79B2/3, PEN2, and MYB34/51/122, and requires functional SAR signaling. Genetic analyses suggest that systemi- cally elevated indoles are dispensable for SAR and associated systemic increases of salicylic acid. However, soil-grown but not hydroponically -cultivated cyp79b2/3 and pen2 plants, both defective in indolic secondary metabolism, exhibit pre-induced immunity, which abrogates their intrinsic ability to induce SAR.展开更多
文摘Jasmonates （JAs） are plant hormones with essential roles in plant defense and development. The basic- helix-loop-helix （bHLH） transcription factor （TF） MYC2 has recently emerged as a master regulator of most aspects of the jasmonate （JA） signaling pathway in Arabidopsis. MYC2 coordinates JA-mediated defense responses by antagonistically regulating two different branches of the JA signaling pathway that determine resistance to pests and pathogens, respectively. MYC2 is required for induced systemic resistance （ISR） triggered by beneficial soil microbes while MYC2 function is targeted by pathogens during effector-mediated suppression of innate immunity in roots. Another notable function of MYC2 is the regulation of crosstalk between the signaling pathways of JA and those of other phytohormones such as abscisic acid （ABA）, salicylic acid （SA）, gibberellins （GAs）, and auxin （IAA）. MYC2 also regulates interactions between JA signaling and light, phytochrome signaling, and the circadian clock, MYC2 is involved in JA-regulated plant development, lateral and adventitious root formation, flowering time, and shade avoidance syndrome. Related bHLH TFs MYC3 and MYC4 also regulate both overlapping and distinct MYC2-regulated functions in Arabidopsis while MYC2 orthologs act as ＇master switches＇ that regulate JA-mediated biosynthesis of secondary metabolites. Here, we briefly review recent studies that revealed mechanistic new insights into the mode of action of this versatile TF.
文摘There is increasing evidence that pathogens do not only elicit direct defense responses, but also cause pronounced changes in primary carbohydrate metabolism. Cell-wall-bound invertases belong to the key regulators of carbohydrate partitioning and source-sink relations. Whereas studies have focused so far only on the transcriptional induction of invertase genes in response to pathogen infection, the role of post-translational regulation of invertase activity has been neglected and was the focus of the present study. Expression analyses revealed that the high mRNA level of one out of three proteinaceous invertase inhibitors in source leaves of Arabidopsis thaliana is strongly repressed upon infection by a virulent strain of Pseudomonas syringae pv. tomato DC3000. This repression is paralleled by a decrease in invertase inhibitor activity. The physiological role of this regulatory mechanism is revealed by the finding that in situ invertase activity was detectable only upon infection by P. syringae. In contrast, a high invertase activity could be measured in vitro in crude and cell wall extracts prepared from both infected and non-infected leaves. The discrepancy between the in situ and in vitro invertase activity of control leaves and the high in situ invertase activity in infected leaves can be explained by the pathogen-dependent repression of invertase inhibitor expression and a concomitant reduction in invertase inhibitor activity. The functional importance of the release of invertase from post-translational inhibition for the defense response was substantiated by the application of the competitive chemical invertase inhibitor acarbose. Posttranslational inhibition of extracellular invertase activity by infiltration of acarbose in leaves was shown to increase the susceptibility to P. syringae. The impact of invertase inhibition on spatial and temporal dynamics of the repression of photosynthesis and promotion of bacterial growth during pathogen infection supports a role for extracellular invertase in plant defen
文摘The Arabidopsis accelerated cell death 6-1 （acd6-1） mutant shows constitutive defense, cell death, and ex- treme dwarf phenotypes. In a screen for acd6-1 suppressors, we identified a mutant that was disrupted by a T-DNA in the PHOSPHATE TRANSPORTER 4;1 （PHT4;1） gene. The suppressor mutant pht4;1-1 is dominant, expresses truncated PHT4;1 transcripts, and is more susceptible to virulent Pseudomonas syringae strains but not to several avirulent strains. Treat- ment with a salicylic acid （SA） agonist induced a similar level of resistance in Col-0 and pht4;1-1, suggesting that PHT4;1 acts upstream of the SA pathway. Genetic analysis further indicates that PHT4,1 contributes to SID2-dependent and -in- dependent pathways. Transgenic expression of the DNA fragment containing the PHT4;1-1 region or the full-length PHT4;1 gene in wild-type conferred enhanced susceptibility to Pseudomonas infection. Interestingly, expression of PHT4;1 is reg- ulated by the circadian clock. Together, these data suggest that the phosphate transporter PHT4;1 is critical for basal defense and also implicate a potential role of the circadian clock in regulating innate immunity of Arabidopsis.
基金This work was funded by The Max Planck Society, an Alexander von Hum-boldt Foundation postdoctoral fellowship, and the National Nature Science Foundation of China （Grant 31770277） （HC）, a Chinese Scholarship Council PhD fellowship （CSC） （JQ） and Deutsche Forschungsgemein- schaft SFB 670 grant （JEP, DB）.
文摘In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.
基金This research was supported, in part, by National Science Foundation grant IOS-1025642 （G,B.M.）,
文摘The Pto protein kinase from Solanum pimpinellifolium interacts with Pseudomonas syringae effectors AvrPto or AvrPtoB to activate effector-triggered immunity. The previously solved crystal structures of the AvrPto-Pto and AvrPtoB-Pto complexes revealed that Pro binds each effector through both a shared and a unique interface. Hera we use natural variation in wild species of tomato to further investigate Pto recognition of these two effectors. One species, Solanum chmielewskU, was found to have many accessions that recognize only AvrPtoB. The Pto ortholog from one of these accessions was responsible for recognition of AvrPtoB and it differed from Solanum pimpinellifolium Pto by only 14 amino acids, including two in the AvrPto-specific interface, glutamate-49/glycine-51. Converting these two residues to those in Pro （histidine-49/valine-51） did not restore recognition of AvrPto. Subsequent experiments revealed that a single substitution of a histidine-to-aspartate at position 193 in Pto, which is not near the AvrPto- specific interface, was sufficient for conferring recognRion of AvrPto in plant cells. The reciprocal substi- tution of aspartate-to-histidine-193 in Pto abolished AvrPto recognition, confirming the importance of this residue. Our results reveal new aspects about effector recognition by Pto and demonstrate the value of using natural variation to understand the interaction between resistance proteins and pathogen effectors.
基金This work was supported by the German Research Foundation （DFG Cluster of Excellence on Plant Sciences and DFG Graduate program IRTG 1525）, and the Swiss National Science Foundation （SNF Grant No, 3100A-125374）.
文摘Tryptophan-derived, indolic metabolites possess diverse functions in Arabidopsis innate immunity to microbial pathogen infection. Hers, we investigate the functional role and regulatory characteristics of indolic metabolism in Arabidopsis systemic acquired resistance （SAR） triggered by the bacterial pathogen Pseudomonas syringae. Indolic metabolism is broadly activated in both P. syringae-inoculated and distant, non-inoculated leaves. At inoculation sites, camalexin, indol-3-ylmethylamine （13A）, and indole-3-carboxylic acid （ICA） are the major accumulating compounds. Camalexin accumulation is positively affected by MYB122, and the cytochrome P450 genes CYP81F1 and CYP81F2. Local 13A production, by contrast, occurs via indole glucosinolate breakdown by PEN2- dependent and independent pathways. Moreover, exogenous application of the defense hormone salicylic acid stimulates 13A generation at the expense of its precursor indol-3-ylmethylglucosinolate （13M）, and the SAR regulator pipecolic acid primes plants for enhanced P. syringae-induced activation of distinct branches of indolic metabolism. In uninfected systemic tissue, the metabolic response is more specific and associated with enhanced levels of the indolics 13A, ICA, and indole-3-carbaldehyde （ICC）. Systemic indole accumulation fully depends on functional CYP79B2/3, PEN2, and MYB34/51/122, and requires functional SAR signaling. Genetic analyses suggest that systemi- cally elevated indoles are dispensable for SAR and associated systemic increases of salicylic acid. However, soil-grown but not hydroponically -cultivated cyp79b2/3 and pen2 plants, both defective in indolic secondary metabolism, exhibit pre-induced immunity, which abrogates their intrinsic ability to induce SAR.
