Recent studies have shown that global translational reprogramming is an early activation event in pattern-triggered immunity,when plants recognize microbe-associated molecular patterns.However,it is not fully known wh...Recent studies have shown that global translational reprogramming is an early activation event in pattern-triggered immunity,when plants recognize microbe-associated molecular patterns.However,it is not fully known whether translational regulation also occurs in subsequent immune responses,such as effector-triggered immunity(ETI).In this study,we performed genome-wide ribosome profiling in Arabidopsis upon RPS2-mediated ETI activation and discovered that specific groups of genes were translationally regulated,mostly in coordination with transcription.These genes encode enzymes involved in aromatic amino acid,phenylpropanoid,camalexin,and sphingolipid metabolism.The functional significance of these components in ETI was confirmed by genetic and biochemical analyses.Our findings provide new insights into diverse translational regulation of plant immune responses and demonstrate that translational coordination of metabolic gene expression is an important strategy for ETI.展开更多
Avirulence effectors(Avrs),encoded by plant pathogens,can be recognized by plants harboring the corresponding resistance proteins,thereby initiating effector-triggered immunity(ETI).In susceptible plants,however,Avrs ...Avirulence effectors(Avrs),encoded by plant pathogens,can be recognized by plants harboring the corresponding resistance proteins,thereby initiating effector-triggered immunity(ETI).In susceptible plants,however,Avrs can function as effectors,facilitating infection via effector-triggered susceptibility(ETS).Mechanisms of Avr-mediated ETS remain largely unexplored.Here we report that the Magnaporthe oryzae effector Avr-PikD enters rice cells via the canonical cytoplasmic secretion pathway and suppresses rice basal defense.Avr-PikD interacts with an LSD1-like transcriptional activator AKIP30 of rice,and AKIP30 is also a positive regulator of rice immunity,whereas Avr-PikD impedes its nuclear localization and suppresses its transcriptional activity.In summary,M.oryzae delivers Avr-PikD into rice cells to facilitate ETS by inhibiting AKIP30-mediated transcriptional regulation of immune response against M.oryzae.展开更多
Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and colonization.If the plant carries resistance(R)proteins that recognize pathogen effectors,effector-...Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and colonization.If the plant carries resistance(R)proteins that recognize pathogen effectors,effector-triggered immunity(ETI)is activated,resulting in a robust immune response and hypersensitive response(HR).The bipartite effector AvrRps4 from Pseudomonas syringae pv.pisi has been well studied in terms of avirulence function.In planta,AvrRps4 is processed into two parts.The Cterminal fragment of AvrRps4(AvrRps4^(C))induces HR in turnip and is recognized by the paired resistance proteins AtRRS1/AtRPS4 in Arabidopsis.Here,we show that AvrRps4^(C)targets a group of Arabidopsis WRKY,including WRKY46,WRKY53,WRKY54,and WRKY70,to induce its virulence function.Indeed,AvrRps4^(C)suppresses the general binding and transcriptional activities of immune-positive regulator WRKY54 and WRKY54-mediated resistance.AvrRps4^(C)interferes with WRKY54's binding activity to target gene SARD1 in vitro,suggesting WRKY54 is sequestered from the SARD1 promoter by AvrRps4^(C).Through the interaction of Avr Rps4^(C)with four WRKYs,AvrRps4 enhances the formation of homo-/heterotypic complexes of four WRKYs and sequesters them in the cytoplasm,thus inhibiting their function in plant immunity.Together,our results provide a detailed virulence mechanism of AvrRps4 through its C-terminus.展开更多
Pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)are required for host defense against pathogens.Although PTI and ETI are intimately connected,the underlying molecular mechanisms remain elusive.In th...Pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)are required for host defense against pathogens.Although PTI and ETI are intimately connected,the underlying molecular mechanisms remain elusive.In this study,we demonstrate that flg22 priming attenuates Pseudomonas syringae pv.tomato DC3000(Pst)AvrRpt2-induced hypersensitive cell death,resistance,and biomass reduction in Arabidopsis.Mitogen-activated protein kinases(MAPKs)are key signaling regulators of PTI and ETI.The absence of MPK3 and MPK6 significantly reduces pre-PTI-mediated ETI suppression(PES).We found that MPK3/MPK6 interact with and phosphorylate the downstream transcription factor WRKY18,which regulates the expression of AP2C1 and PP2C5,two genes encoding protein phosphatases.Furthermore,we observed that the PTI-suppressed ETI-triggered cell death,MAPK activation,and growth retardation are significantly attenuated in wrky18/40/60 and ap2c1 pp2c5 mutants.Taken together,our results suggest that the MPK3/MPK6-WRKYs-PP2Cs module underlies PES and is essential for the maintenance of plant fitness during ETI.展开更多
After three decades of the amazing progress made on molecular studies of plant-microbe interactions(MPMI),we have begun to ask ourselves"what are the major questions still remaining?"as if the puzzle has onl...After three decades of the amazing progress made on molecular studies of plant-microbe interactions(MPMI),we have begun to ask ourselves"what are the major questions still remaining?"as if the puzzle has only a few pieces missing.Such an exercise has ultimately led to the realization that we still have many more questions than answers.Therefore,it would be an impossible task for us to project a coherent"big picture"of the MPMI field in a single review.Instead,we provide our opinions on where we would like to go in our research as an invitation to the community to join us in this exploration of new MPMI frontiers.展开更多
Plant pathogens deliver effector proteins that alter host processes to create an environment conducive to colonization. Attention has focused on identifying the targets of effectors and how their manipulation facil- i...Plant pathogens deliver effector proteins that alter host processes to create an environment conducive to colonization. Attention has focused on identifying the targets of effectors and how their manipulation facil- itates disease. RXLR effector Pi04089 from the potato blight pathogen Phytophthora infestans accumu- lates in the host nucleus and enhances colonization when transiently expressed in planta. Its nuclear local- ization is required for enhanced P. infestans colonization. Pi04089 interacts in yeast and in planta with a putative potato K-homology （KH） RNA-binding protein, StKRBPI. Co-localization of Pi04089 and StKRBP1, and bimolecular fluorescence complementation between them, indicate they associate at nuclear speckles. StKRBP1 protein levels increased when it was co-expressed with Pi04089. Indeed, such accumu- lation of StKRBP1 was observed also on the first day of leaf colonization by the pathogen. Remarkably, overexpression of StKRBP1 significantly enhances P. infestans infection. Mutation of the nucleotide- binding motif GxxG to GDDG in all three KH domains of StKRBP1 abolishes its interaction with Pi04089, its localization to nuclear speckles, and its increased accumulation when co-expressed with the effector. Moreover, the mutant StKRBP1 protein no longer enhances leaf colonization by P. infestans, implying that nucleotide binding is likely required for this activity. We thus argue that StKRBP1 can be regarded as a sus- ceptibility factor, as its activity is beneficial to the pathogen.展开更多
The interaction between plants and pathogens represents a dynamic competition between a robust immune system and efficient infectious strategies. Plant innate immunity is composed of complex and highly regulated molec...The interaction between plants and pathogens represents a dynamic competition between a robust immune system and efficient infectious strategies. Plant innate immunity is composed of complex and highly regulated molecular networks, which can be triggered by the perception of either conserved or race-specific pathogenic molecular signatures. Small RNAs are emerging as versatile regulators of plant development, growth and response to biotic and abiotic stresses. They act in different tiers of plant immunity, including the pathogen-associated molecular pattern-triggered and the effector-triggered immunity. On the other hand, pathogens have evolved effector molecules to suppress or hijack the host small RNA pathways. This leads to an arms race between plants and pathogens at the level of small RNA-mediated defense. Here, we review recent advances in small RNA-mediated defense responses and discuss the challenging questions in this area.展开更多
Plant pathogenic bacteria deliver effectors into plant cells to suppress immunity and promote pathogen survival;however, these effectors can be recognised by plant disease resistance (R) proteins to activate innate im...Plant pathogenic bacteria deliver effectors into plant cells to suppress immunity and promote pathogen survival;however, these effectors can be recognised by plant disease resistance (R) proteins to activate innate immunity. The bacterial acetyltransferase effectors HopZ5 and AvrBsT trigger immunity in Arabidopsis thaliana genotypes lacking SUPPRESSOR OF AVRBST-ELICITED RESISTANCE 1 (SOBER1). Using an Arabidopsis accession, Tscha-1, that naturally lacks functional SOBER1 but is unable to recognise HopZ5, we demonstrate that RESISTANCE TO P. SYRINGAE PV MACULICOLA 1 (RPM1) and RPM1-INTERACTING PROTEIN 4 (RIN4) are indispensable for HopZ5- or AvrBsT-triggered immunity. Remarkably, T166 of RIN4, the phosphorylation of which is induced by AvrB and AvrRpm1, was directly acetylated by HopZ5 and AvrBsT. Furthermore, we demonstrate that the acetylation of RIN4 T166 is required and sufficient for HopZ5- or AvrBsT-triggered RPM1-dependent defence activation. Finally, we show that SOBER1 interferes with HopZ5- or AvrBsT-triggered immunity by deacetylating RIN4 T166. We have thus elucidated detailed molecular mechanisms underlying the activation and suppression of plant innate immunity triggered by two bacterial acetyltransferases, HopZ5 and AvrBsT from different bacterial pathogens.展开更多
Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates p...Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates plant growth and defense in both compatible and incompatible infections.This module consisted of BZR1,a key transcription factor in brassinosteroid(BR)signaling,and EDS1,an essential positive regulator of plant innate immunity.We found that EDS1 interacts with BZR1 and suppresses its transcriptional activ-ities.Consistently,upregulation of EDS1 function by a virulent Pseudomonas syringae strain or salicylic acid treatment inhibited BZR1-regulated expression of BR-responsive genes and BR-promoted growth.Furthermore,we showed that the cytoplasmic fraction of BZR1 positively regulates effector-triggered im-munity(ETI)controlled by the TIR-NB-LRR protein RPS4,which is attenuated by BZR1's nuclear transloca-tion.Mechanistically,cytoplasmic BZR1 facilitated AvrRps4-triggered dissociation of EDS1 and RPS4 by binding to EDS1,thus leading to efficient activation of RPS4-controlled ETI.Notably,transgenic expression of a mutant BZR1 that accumulates exclusively in the cytoplasm improved pathogen resistance without compromising plant growth.Collectively,these results shed new light on plant growth-defense coordina-tion and reveal a previously unknown function for the cytoplasmic fraction of BZR1.The BZR1-EDS1 mod-ule may be harnessed for the simultaneous improvement of crop productivity and pathogen resistance.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
Recognition of a pathogen by the plant immune system often triggers a form of regulated cell death traditionally known as the hypersensitive response(HR).This type of cell death occurs precisely at the site of pathoge...Recognition of a pathogen by the plant immune system often triggers a form of regulated cell death traditionally known as the hypersensitive response(HR).This type of cell death occurs precisely at the site of pathogen recognition,and it is restricted to a few cells.Extensive research has shed light on how plant immune receptors are mechanistically activated.However,two central key questions remain largely unresolved:how does cell death zonation take place,and what are the mechanisms that underpin this phenomenon?Consequently,bona fide transcriptional indicators of HR are lacking,which prevents deeper insight into its mechanisms before cell death becomes macroscopic and precludes early or live observation.In this study,to identify the transcriptional indicators of HR we used the paradigmatic Arabidopsis thaliana–Pseudomonas syringae pathosystem and performed a spatiotemporally resolved gene expression analysis that compared infected cells that will undergo HR upon pathogen recognition with bystander cells that will stay alive and activate immunity.Our data revealed unique and time-dependent differences in the repertoire of differentially expressed genes,expression profiles,and biological processes derived from tissue undergoing HR and that of its surroundings.Furthermore,we generated a pipeline based on concatenated pairwise comparisons between time,zone,and treatment that enabled us to define 13 robust transcriptional HR markers.Among these genes,the promoter of an uncharacterized AAA-ATPase was used to obtain a fluorescent reporter transgenic line that displays a strong spatiotemporally resolved signal specifically in cells that will later undergo pathogen-triggered cell death.This valuable set of genes can be used to define cells that are destined to die upon infection with HR-triggering bacteria,opening new avenues for specific and/or high-throughput techniques to study HR processes at a single-cell level.展开更多
基金This study was supported by grants from NIH R35GM118036-02,NSF IOS 1645589,and HHMI-GBMF(grant no.GBMF3032)to X.D.and a Hargitt fellowship to H.Y.
文摘Recent studies have shown that global translational reprogramming is an early activation event in pattern-triggered immunity,when plants recognize microbe-associated molecular patterns.However,it is not fully known whether translational regulation also occurs in subsequent immune responses,such as effector-triggered immunity(ETI).In this study,we performed genome-wide ribosome profiling in Arabidopsis upon RPS2-mediated ETI activation and discovered that specific groups of genes were translationally regulated,mostly in coordination with transcription.These genes encode enzymes involved in aromatic amino acid,phenylpropanoid,camalexin,and sphingolipid metabolism.The functional significance of these components in ETI was confirmed by genetic and biochemical analyses.Our findings provide new insights into diverse translational regulation of plant immune responses and demonstrate that translational coordination of metabolic gene expression is an important strategy for ETI.
基金supported by grants from the National Natural Science Foundation of China(31401692,31901960,32272513,32001976)the Natural Science Foundation of Fujian Province(2019J01766,2023J011418,2020J05177)+3 种基金Fujian Provincial Science and Technology Key Project(2022NZ030014)External Cooperation Program of Fujian Academy of Agricultural Sciences(DWHZ-2024-23)State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crop Opening Project(SKL2019005)Project of Fujian Provincial Department of Education(JAT190627)。
文摘Avirulence effectors(Avrs),encoded by plant pathogens,can be recognized by plants harboring the corresponding resistance proteins,thereby initiating effector-triggered immunity(ETI).In susceptible plants,however,Avrs can function as effectors,facilitating infection via effector-triggered susceptibility(ETS).Mechanisms of Avr-mediated ETS remain largely unexplored.Here we report that the Magnaporthe oryzae effector Avr-PikD enters rice cells via the canonical cytoplasmic secretion pathway and suppresses rice basal defense.Avr-PikD interacts with an LSD1-like transcriptional activator AKIP30 of rice,and AKIP30 is also a positive regulator of rice immunity,whereas Avr-PikD impedes its nuclear localization and suppresses its transcriptional activity.In summary,M.oryzae delivers Avr-PikD into rice cells to facilitate ETS by inhibiting AKIP30-mediated transcriptional regulation of immune response against M.oryzae.
基金supported by Basic Science Research Program and LAMP Program through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(No.2021R1I1A3054417,2022R1I1A1A01063394,RS-2023-00301974)the National Research Foundation of Korea(NRF)grant funded by the Korea government(MSIT)(No.2021M3A9I5023695,2022R1A5A1031361)grants from the New Breeding Technologies Development Program(RS-2024-00322125),Rural Development Administration,Republic of Korea。
文摘Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and colonization.If the plant carries resistance(R)proteins that recognize pathogen effectors,effector-triggered immunity(ETI)is activated,resulting in a robust immune response and hypersensitive response(HR).The bipartite effector AvrRps4 from Pseudomonas syringae pv.pisi has been well studied in terms of avirulence function.In planta,AvrRps4 is processed into two parts.The Cterminal fragment of AvrRps4(AvrRps4^(C))induces HR in turnip and is recognized by the paired resistance proteins AtRRS1/AtRPS4 in Arabidopsis.Here,we show that AvrRps4^(C)targets a group of Arabidopsis WRKY,including WRKY46,WRKY53,WRKY54,and WRKY70,to induce its virulence function.Indeed,AvrRps4^(C)suppresses the general binding and transcriptional activities of immune-positive regulator WRKY54 and WRKY54-mediated resistance.AvrRps4^(C)interferes with WRKY54's binding activity to target gene SARD1 in vitro,suggesting WRKY54 is sequestered from the SARD1 promoter by AvrRps4^(C).Through the interaction of Avr Rps4^(C)with four WRKYs,AvrRps4 enhances the formation of homo-/heterotypic complexes of four WRKYs and sequesters them in the cytoplasm,thus inhibiting their function in plant immunity.Together,our results provide a detailed virulence mechanism of AvrRps4 through its C-terminus.
基金supported by grants from the National Key Research and Development Project(2022YFE0198100)National Natural Science Foundation of China(32172420)+2 种基金Natural Science Foundation of Jiangsu Province(SBK20220085)Fundamental Research Funds for the Central Universities(KYXK202009,ZJ21195012)the Startup Fund for Distinguished Scholars from Nanjing Agricultural University(to Y.W.).
文摘Pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)are required for host defense against pathogens.Although PTI and ETI are intimately connected,the underlying molecular mechanisms remain elusive.In this study,we demonstrate that flg22 priming attenuates Pseudomonas syringae pv.tomato DC3000(Pst)AvrRpt2-induced hypersensitive cell death,resistance,and biomass reduction in Arabidopsis.Mitogen-activated protein kinases(MAPKs)are key signaling regulators of PTI and ETI.The absence of MPK3 and MPK6 significantly reduces pre-PTI-mediated ETI suppression(PES).We found that MPK3/MPK6 interact with and phosphorylate the downstream transcription factor WRKY18,which regulates the expression of AP2C1 and PP2C5,two genes encoding protein phosphatases.Furthermore,we observed that the PTI-suppressed ETI-triggered cell death,MAPK activation,and growth retardation are significantly attenuated in wrky18/40/60 and ap2c1 pp2c5 mutants.Taken together,our results suggest that the MPK3/MPK6-WRKYs-PP2Cs module underlies PES and is essential for the maintenance of plant fitness during ETI.
基金grants from the National Institutes of Health(NIH 1R35GM118036)National Science Foundation(IOS 1645589)+5 种基金Howard Hughes Medical Institute to X.D.,grants from the NIH(NIH 1R35GM136402)National Science Foundation(NSF 1937855-0)United States Department of Agriculture(USDA,2019-70016-2979)G.C.,a grant from National Natural Science Foundation of China(31830019)J.-M.Z.,and a grant from National Natural Science Foundation of China(31922075)Youth Innovation Promotion Association of the Chinese Academy of Sciences to J.Z.
文摘After three decades of the amazing progress made on molecular studies of plant-microbe interactions(MPMI),we have begun to ask ourselves"what are the major questions still remaining?"as if the puzzle has only a few pieces missing.Such an exercise has ultimately led to the realization that we still have many more questions than answers.Therefore,it would be an impossible task for us to project a coherent"big picture"of the MPMI field in a single review.Instead,we provide our opinions on where we would like to go in our research as an invitation to the community to join us in this exploration of new MPMI frontiers.
文摘Plant pathogens deliver effector proteins that alter host processes to create an environment conducive to colonization. Attention has focused on identifying the targets of effectors and how their manipulation facil- itates disease. RXLR effector Pi04089 from the potato blight pathogen Phytophthora infestans accumu- lates in the host nucleus and enhances colonization when transiently expressed in planta. Its nuclear local- ization is required for enhanced P. infestans colonization. Pi04089 interacts in yeast and in planta with a putative potato K-homology （KH） RNA-binding protein, StKRBPI. Co-localization of Pi04089 and StKRBP1, and bimolecular fluorescence complementation between them, indicate they associate at nuclear speckles. StKRBP1 protein levels increased when it was co-expressed with Pi04089. Indeed, such accumu- lation of StKRBP1 was observed also on the first day of leaf colonization by the pathogen. Remarkably, overexpression of StKRBP1 significantly enhances P. infestans infection. Mutation of the nucleotide- binding motif GxxG to GDDG in all three KH domains of StKRBP1 abolishes its interaction with Pi04089, its localization to nuclear speckles, and its increased accumulation when co-expressed with the effector. Moreover, the mutant StKRBP1 protein no longer enhances leaf colonization by P. infestans, implying that nucleotide binding is likely required for this activity. We thus argue that StKRBP1 can be regarded as a sus- ceptibility factor, as its activity is beneficial to the pathogen.
基金funded by the grant from National Basic Research Program of China (973 Program, 2012CB910503) to Hai Huangby the Gordon and Betty Moore Foundation through Grant GBMF 2550.02 to the Life Sciences Research Foundation to Li Yang
文摘The interaction between plants and pathogens represents a dynamic competition between a robust immune system and efficient infectious strategies. Plant innate immunity is composed of complex and highly regulated molecular networks, which can be triggered by the perception of either conserved or race-specific pathogenic molecular signatures. Small RNAs are emerging as versatile regulators of plant development, growth and response to biotic and abiotic stresses. They act in different tiers of plant immunity, including the pathogen-associated molecular pattern-triggered and the effector-triggered immunity. On the other hand, pathogens have evolved effector molecules to suppress or hijack the host small RNA pathways. This leads to an arms race between plants and pathogens at the level of small RNA-mediated defense. Here, we review recent advances in small RNA-mediated defense responses and discuss the challenging questions in this area.
基金This research was supported by Basic Science Research Programs through the National Research Foundation of Korea(NRF)funded by the Ministry of Education(NRF-2019R1I1A1A01060108)Korean government(MSIT)(NRF-2018R1A5A1023599 and NRF-2019R1A2C2084705)。
文摘Plant pathogenic bacteria deliver effectors into plant cells to suppress immunity and promote pathogen survival;however, these effectors can be recognised by plant disease resistance (R) proteins to activate innate immunity. The bacterial acetyltransferase effectors HopZ5 and AvrBsT trigger immunity in Arabidopsis thaliana genotypes lacking SUPPRESSOR OF AVRBST-ELICITED RESISTANCE 1 (SOBER1). Using an Arabidopsis accession, Tscha-1, that naturally lacks functional SOBER1 but is unable to recognise HopZ5, we demonstrate that RESISTANCE TO P. SYRINGAE PV MACULICOLA 1 (RPM1) and RPM1-INTERACTING PROTEIN 4 (RIN4) are indispensable for HopZ5- or AvrBsT-triggered immunity. Remarkably, T166 of RIN4, the phosphorylation of which is induced by AvrB and AvrRpm1, was directly acetylated by HopZ5 and AvrBsT. Furthermore, we demonstrate that the acetylation of RIN4 T166 is required and sufficient for HopZ5- or AvrBsT-triggered RPM1-dependent defence activation. Finally, we show that SOBER1 interferes with HopZ5- or AvrBsT-triggered immunity by deacetylating RIN4 T166. We have thus elucidated detailed molecular mechanisms underlying the activation and suppression of plant innate immunity triggered by two bacterial acetyltransferases, HopZ5 and AvrBsT from different bacterial pathogens.
基金supported by grants from the National Natural Science Foundation of China(91935304)the Innovative Postdoctoral Research Initiative of Henan Province(to G.Q.)the National Science Foundation(EAGER grant 1464527 and grant IOS-1758994 to Z.Q.F.).
文摘Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates plant growth and defense in both compatible and incompatible infections.This module consisted of BZR1,a key transcription factor in brassinosteroid(BR)signaling,and EDS1,an essential positive regulator of plant innate immunity.We found that EDS1 interacts with BZR1 and suppresses its transcriptional activ-ities.Consistently,upregulation of EDS1 function by a virulent Pseudomonas syringae strain or salicylic acid treatment inhibited BZR1-regulated expression of BR-responsive genes and BR-promoted growth.Furthermore,we showed that the cytoplasmic fraction of BZR1 positively regulates effector-triggered im-munity(ETI)controlled by the TIR-NB-LRR protein RPS4,which is attenuated by BZR1's nuclear transloca-tion.Mechanistically,cytoplasmic BZR1 facilitated AvrRps4-triggered dissociation of EDS1 and RPS4 by binding to EDS1,thus leading to efficient activation of RPS4-controlled ETI.Notably,transgenic expression of a mutant BZR1 that accumulates exclusively in the cytoplasm improved pathogen resistance without compromising plant growth.Collectively,these results shed new light on plant growth-defense coordina-tion and reveal a previously unknown function for the cytoplasmic fraction of BZR1.The BZR1-EDS1 mod-ule may be harnessed for the simultaneous improvement of crop productivity and pathogen resistance.
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.
文摘Recognition of a pathogen by the plant immune system often triggers a form of regulated cell death traditionally known as the hypersensitive response(HR).This type of cell death occurs precisely at the site of pathogen recognition,and it is restricted to a few cells.Extensive research has shed light on how plant immune receptors are mechanistically activated.However,two central key questions remain largely unresolved:how does cell death zonation take place,and what are the mechanisms that underpin this phenomenon?Consequently,bona fide transcriptional indicators of HR are lacking,which prevents deeper insight into its mechanisms before cell death becomes macroscopic and precludes early or live observation.In this study,to identify the transcriptional indicators of HR we used the paradigmatic Arabidopsis thaliana–Pseudomonas syringae pathosystem and performed a spatiotemporally resolved gene expression analysis that compared infected cells that will undergo HR upon pathogen recognition with bystander cells that will stay alive and activate immunity.Our data revealed unique and time-dependent differences in the repertoire of differentially expressed genes,expression profiles,and biological processes derived from tissue undergoing HR and that of its surroundings.Furthermore,we generated a pipeline based on concatenated pairwise comparisons between time,zone,and treatment that enabled us to define 13 robust transcriptional HR markers.Among these genes,the promoter of an uncharacterized AAA-ATPase was used to obtain a fluorescent reporter transgenic line that displays a strong spatiotemporally resolved signal specifically in cells that will later undergo pathogen-triggered cell death.This valuable set of genes can be used to define cells that are destined to die upon infection with HR-triggering bacteria,opening new avenues for specific and/or high-throughput techniques to study HR processes at a single-cell level.
