The wall-associated kinases(WAKs)play a crucial role in rice resistance,but their relationship to yield-related traits remains poorly understood.In this study,we analyzed the rice wall-associated kinase galacturonan-b...The wall-associated kinases(WAKs)play a crucial role in rice resistance,but their relationship to yield-related traits remains poorly understood.In this study,we analyzed the rice wall-associated kinase galacturonan-binding(WAKg)gene family and evaluated its association with both disease resistance and grain yield.A total of 108 OsWAKg genes were identified in rice.Promoter cis-element analysis revealed that the promoter regions of OsWAKg genes contain abundant resistance-and hormone-related elements.Induced expression analysis of 18 OsWAKg genes highly expressed in both rice leaves and roots showed that 14 genes were pathogen-induced,9 were induced by development-related hormones,and 8 were responded to both stimuli.Transgenic validation confirmed that OsWAKg16 and OsWAKg52 positively regulate rice disease resistance and yield.Moreover,OsWAKg52 regulates rice disease resistance through multiple pattern-triggered immunity responses.These findings demonstrate that OsWAKgs significantly contribute to the coordinated regulation of disease resistance and grain yield,providing new insights into rice WAKg gene family and potential genetic resources for synergistic crop improvement.展开更多
Plants recognize microbe-associated molecular patterns(MAMPs)to activate immune responses and defense priming to defend against pathogen infections.Transcriptional regulation of gene expression is crucial for plant im...Plants recognize microbe-associated molecular patterns(MAMPs)to activate immune responses and defense priming to defend against pathogen infections.Transcriptional regulation of gene expression is crucial for plant immunity and is mediated by multiple factors,including DNA methylation.However,it remains unknown whether and how DNA demethylation contributes to immune responses in MAMPtriggered immunity.Here,we report that active DNA demethylation is required for MAMP-triggered immunity to bacterial pathogens.The rdd-2 triple mutant carrying mutations in ROS1,DML2,and DML3 that encode DNA glycosylases,which are key DNA demethylation enzymes,exhibits compromised immune responses triggered by the MAMPs fig22 and elf18.Genome-wide methylome analysis reveals that fig22 induces rapid and specific DNA demethylation in an RDD-dependent manner.The expression levels of salicylic acid signaling-related and phytoalexin biosynthesis-related genes are tightly associated with the fig22-induced promoter demethylation.The compromised accumulation of priming compounds and antimicrobial metabolites ultimately leads to a defense priming defect in the rdd-2 mutant.Our results reveal the critical role of active DNA demethylation in the MAMP-triggered immune response and provide unique insight into the molecular mechanism of fig22-modulated DNA demethylation.展开更多
The flagellin-sensing mechanism is one of the most extensively studied topics in plant defense systems.This widespread interest arises from the ability of flagellin to trigger robust and extensive responses,establishi...The flagellin-sensing mechanism is one of the most extensively studied topics in plant defense systems.This widespread interest arises from the ability of flagellin to trigger robust and extensive responses,establishing it as a cornerstone for research into other defense mechanisms.Plants recognize bacterial flagellin epitopes through plasma-membrane-localized pattern-recognition receptors,initiating pattern-triggered immunity as the frontline defense against bacterial pathogens.In this review,we comprehensively summarize flagellin-sensing mechanisms and signal transduction pathways in plants.We compare the flagellin-sensing mechanisms of plants and mammals,focusing on epitope processing and recognition.We present detailed downstream signaling events,from receptor complex formation to transcriptional reprogramming.Furthermore,we highlight the evolutionary arms race between plants and bacteria and incorporate emerging insights into how flagellin-triggered responses are modulated by receptor networking,phytocytokines,and environmental factors.These findings suggest that flagellin-mediated immune responses are highly dynamic and context dependent.By synthesizing current knowledge and recent discoveries,this review provides updated perspectives on plant–microbe interactions and aims to inspire future research in plant immunity.展开更多
Beyond their function as structural barriers,plant cell walls are essential elements for the adaptation of plants to environmental conditions.Cell walls are dynamic structures whose composition and integrity can be al...Beyond their function as structural barriers,plant cell walls are essential elements for the adaptation of plants to environmental conditions.Cell walls are dynamic structures whose composition and integrity can be altered in response to environmental challenges and developmental cues.These wall changes are perceived by plant sensors/receptors to trigger adaptative responses during development and upon stress perception.Plant cell wall damage caused by pathogen infection,wounding,or other stresses leads to the release of wall molecules,such as carbohydrates(glycans),that function as damage-associated molecular patterns(DAMPs).DAMPs are perceived by the extracellular ectodomains(ECDs)of pattern recognition receptors(PRRs)to activate pattern-triggered immunity(PTI)and disease resistance.Similarly,glycans released from the walls and extracellular layers of microorganisms interacting with plants are recognized as microbe-associated molecular patterns(MAMPs)by specific ECD-PRRs triggering PTI responses.The number of oligosaccharides DAMPs/MAMPs identified that are perceived by plants has increased in recent years.However,the structural mechanisms underlying glycan recognition by plant PRRs remain limited.Currently,this knowledge is mainly focused on receptors of the LysM-PRR family,which are involved in the perception of various molecules,such as chitooligosaccharides from fungi and lipo-chitooligosaccharides(i.e.,Nod/MYC factors from bacteria and mycorrhiza,respectively)that trigger differential physiological responses.Nevertheless,additional families of plant PRRs have recently been implicated in oligosaccharide/polysaccharide recognition.These include receptor kinases(RKs)with leucine-rich repeat and Malectin domains in their ECDs(LRR-MAL RKs),Catharanthus roseus RECEPTOR-LIKE KINASE 1-LIKE group(CrRLK1L)with Malectin-like domains in their ECDs,as well as wall-associated kinases,lectin-RKs,and LRR-extensins.The characterization of structural basis of glycans recognition by these new plant receptors will shed light on their similarities with those of mammalians involved in glycan perception.The gained knowledge holds the potential to facilitate the development of sustainable,glycan-based crop protection solutions.展开更多
In plant immunity,a well-orchestrated cascade is initiated by the dimerization of receptor-like kinases(RLKs),followed by the phosphorylation of receptor-like cytoplasmic kinases(RLCKs)and subsequent activation of NAD...In plant immunity,a well-orchestrated cascade is initiated by the dimerization of receptor-like kinases(RLKs),followed by the phosphorylation of receptor-like cytoplasmic kinases(RLCKs)and subsequent activation of NADPH oxidases for ROS generation.Recent findings by Zhong et al.illustrated that a maize signaling module comprising ZmWAKLZmWIK-ZmBLK1-ZmRBOH4 governs quantitative disease resistance to grey leaf spot,a pervasive fungal disease in maize worldwide,unveiling the conservation of this signaling quartet in plant immunity.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
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
In plants,the antagonism between growth and defense is hardwired by hormonal signaling.The perception of pathogen-associatedmolecularpatterns(PAMPs)frominvadingmicroorganismsinhibits auxin signalingand plant growth.Co...In plants,the antagonism between growth and defense is hardwired by hormonal signaling.The perception of pathogen-associatedmolecularpatterns(PAMPs)frominvadingmicroorganismsinhibits auxin signalingand plant growth.Conversely,pathogens manipulate auxin signaling to promote disease,but how this hormone inhibits immunity is not fully understood.Ustilago maydis is a maize pathogen that induces auxin signaling in its host.We characterized a U.maydis effector protein,Naked1(Nkd1),that is translocated into the host nucleus.Through its native ethylene-responsive element binding factor-associated amphiphilic repression(EAR)motif,Nkd1 binds to the transcriptional co-repressors TOPLESS/TOPLESS-related(TPL/TPRs)and prevents the recruitment of a transcriptional repressor involved in hormonal signaling,leading to the derepression of auxin and jasmonate signaling and thereby promoting susceptibility to(hemi)biotrophic pathogens.A moderate upregulation of auxin signaling inhibits the PAMP-triggered reactive oxygen species(ROS)burst,an early defense response.Thus,our findings establish a clear mechanism for auxin-induced pathogen susceptibility.Engineered Nkd1 variants with increased expression or increased EAR-mediated TPL/TPR binding trigger typical salicylic-acid-mediated defense reactions,leading to pathogen resistance.This implies that moderate binding of Nkd1 to TPL is a result of a balancing evolutionary selection process to enable TPL manipulation while avoiding host recognition.展开更多
Plant plasma membrane-resident immune receptors regulate plant immunity by recognizing microbe-associated molecular patterns(MAMPs),damage-associated molecular patterns(DAMPs),and phytocytokines.Phytocytokines are pla...Plant plasma membrane-resident immune receptors regulate plant immunity by recognizing microbe-associated molecular patterns(MAMPs),damage-associated molecular patterns(DAMPs),and phytocytokines.Phytocytokines are plant endogenous peptides,which are usually produced in the cytosol and released into the apoplast when plant encounters pathogen infections.Phytocytokines regulate plant immunity through activating an overlapping signaling pathway with MAMPs/DAMPs with some unique features.Here,we highlight the current understanding of phytocytokine production,perception and functions in plant immunity,and discuss how plants and pathogens manipulate phytocytokine signaling for their own benefits during the plant-pathogen warfare.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
Mitogen-activated protein kinase(MAPK) cascades play pivotal roles in plant defense against phytopathogens downstream of immune receptor complexes. The amplitude and duration of MAPK activation must be strictly contro...Mitogen-activated protein kinase(MAPK) cascades play pivotal roles in plant defense against phytopathogens downstream of immune receptor complexes. The amplitude and duration of MAPK activation must be strictly controlled, but the underlying mechanism remains unclear. Here, we identified Arabidopsis CPL1(C-terminal domain phosphatase-like 1)as a negative regulator of microbe-associated molecular pattern(MAMP)-triggered immunity via a forward-genetic screen. Disruption of CPL1 significantly enhanced plant resistance to Pseudomonas pathogens induced by the bacterial peptide fg22. Furthermore, fg22-induced MPK3/MPK4/MPK6 phosphorylation was dramatically elevated in cpl1 mutants but severely impaired in CPL1 overexpression lines, suggesting that CPL1 might interfere with fg22-induced MAPK activation. Indeed, CPL1 directly interacted with MPK3 and MPK6, as well as the upstream MKK4 and MKK5. A firefy luciferase-based complementation assay indicated that the interaction between MKK4/MKK5 and MPK3/MPK6 was significantly reduced in the presence of CPL1. These results suggest that CPL1 plays a novel regulatory role in suppressing MAMP-induced MAPK cascade activation and MAMP-triggered immunity to bacterial pathogens.展开更多
基金partly granted from the National Natural Science Foundation of China(Grant Nos.32470391 and 32401801)the Joint Open Competitive Project of the Yazhou Bay Laboratory and the China National Seed Company Limited(Grant No.B23YQ1515)+1 种基金the International Cooperation Projects in Hubei Province,China(Grant No.2023EHA045)the Natural Science Foundation of Wuhan University of Bioengineering,China(Grant No.2024KQ07).
文摘The wall-associated kinases(WAKs)play a crucial role in rice resistance,but their relationship to yield-related traits remains poorly understood.In this study,we analyzed the rice wall-associated kinase galacturonan-binding(WAKg)gene family and evaluated its association with both disease resistance and grain yield.A total of 108 OsWAKg genes were identified in rice.Promoter cis-element analysis revealed that the promoter regions of OsWAKg genes contain abundant resistance-and hormone-related elements.Induced expression analysis of 18 OsWAKg genes highly expressed in both rice leaves and roots showed that 14 genes were pathogen-induced,9 were induced by development-related hormones,and 8 were responded to both stimuli.Transgenic validation confirmed that OsWAKg16 and OsWAKg52 positively regulate rice disease resistance and yield.Moreover,OsWAKg52 regulates rice disease resistance through multiple pattern-triggered immunity responses.These findings demonstrate that OsWAKgs significantly contribute to the coordinated regulation of disease resistance and grain yield,providing new insights into rice WAKg gene family and potential genetic resources for synergistic crop improvement.
基金supported by the National Natural Science Foundation of China (31770278, 31970125 to B.L.)Fundamental Research Funds for the Central Universities, Huazhong Agricultural University Scientific & Technological Self-innovation Foundation (2021ZKPY011, 2017RC001 to B.L.)
文摘Plants recognize microbe-associated molecular patterns(MAMPs)to activate immune responses and defense priming to defend against pathogen infections.Transcriptional regulation of gene expression is crucial for plant immunity and is mediated by multiple factors,including DNA methylation.However,it remains unknown whether and how DNA demethylation contributes to immune responses in MAMPtriggered immunity.Here,we report that active DNA demethylation is required for MAMP-triggered immunity to bacterial pathogens.The rdd-2 triple mutant carrying mutations in ROS1,DML2,and DML3 that encode DNA glycosylases,which are key DNA demethylation enzymes,exhibits compromised immune responses triggered by the MAMPs fig22 and elf18.Genome-wide methylome analysis reveals that fig22 induces rapid and specific DNA demethylation in an RDD-dependent manner.The expression levels of salicylic acid signaling-related and phytoalexin biosynthesis-related genes are tightly associated with the fig22-induced promoter demethylation.The compromised accumulation of priming compounds and antimicrobial metabolites ultimately leads to a defense priming defect in the rdd-2 mutant.Our results reveal the critical role of active DNA demethylation in the MAMP-triggered immune response and provide unique insight into the molecular mechanism of fig22-modulated DNA demethylation.
基金supported by grants from the Institute for Basic Science(IBS-R021-D1-2025-a00)the National Research Foundation of Korea(RS-2024-00338015)to H.-S.L.and by the Startup Fund from Duke Kunshan University to E.Y.K.D.-H.Lsupported by a postdoctoral fellowship from the National Research Foundation of Korea(NRF-2021R1A6A3A03039464).No conflict of interest is declared.
文摘The flagellin-sensing mechanism is one of the most extensively studied topics in plant defense systems.This widespread interest arises from the ability of flagellin to trigger robust and extensive responses,establishing it as a cornerstone for research into other defense mechanisms.Plants recognize bacterial flagellin epitopes through plasma-membrane-localized pattern-recognition receptors,initiating pattern-triggered immunity as the frontline defense against bacterial pathogens.In this review,we comprehensively summarize flagellin-sensing mechanisms and signal transduction pathways in plants.We compare the flagellin-sensing mechanisms of plants and mammals,focusing on epitope processing and recognition.We present detailed downstream signaling events,from receptor complex formation to transcriptional reprogramming.Furthermore,we highlight the evolutionary arms race between plants and bacteria and incorporate emerging insights into how flagellin-triggered responses are modulated by receptor networking,phytocytokines,and environmental factors.These findings suggest that flagellin-mediated immune responses are highly dynamic and context dependent.By synthesizing current knowledge and recent discoveries,this review provides updated perspectives on plant–microbe interactions and aims to inspire future research in plant immunity.
基金supported by grant PID2021-126006OB-I00 to A.M.and L.J.grant PID20220-113588RB-I00 to S.M.-S+6 种基金funded by MCIN/AEI/10.13039/501100011033by ERDF A way of making Europe.D.J.B.supported by PRE2019-091276 and P.F.-C.by postdoctoral fellowships financially supported by the Severo Ochoa Program for Centres of Excellence in R&D(grants SEV-2016-0672 and CEX2020-000999-S)funded by MCIN/AEI/10.13039/501100011033.M.M.-D.was recipient of PhD fellow(PRE2019-08812)funded by MCIN/AEI/10.13039/501100011033.E.G.-Rwas supported by Autonomous Region of Madrid fellowship(S2017/BMD-3673)the European Commission-Next Generation EU(Regulation EU2020/2094)through CSIC’s Global Health Platform PTI Salud Global.
文摘Beyond their function as structural barriers,plant cell walls are essential elements for the adaptation of plants to environmental conditions.Cell walls are dynamic structures whose composition and integrity can be altered in response to environmental challenges and developmental cues.These wall changes are perceived by plant sensors/receptors to trigger adaptative responses during development and upon stress perception.Plant cell wall damage caused by pathogen infection,wounding,or other stresses leads to the release of wall molecules,such as carbohydrates(glycans),that function as damage-associated molecular patterns(DAMPs).DAMPs are perceived by the extracellular ectodomains(ECDs)of pattern recognition receptors(PRRs)to activate pattern-triggered immunity(PTI)and disease resistance.Similarly,glycans released from the walls and extracellular layers of microorganisms interacting with plants are recognized as microbe-associated molecular patterns(MAMPs)by specific ECD-PRRs triggering PTI responses.The number of oligosaccharides DAMPs/MAMPs identified that are perceived by plants has increased in recent years.However,the structural mechanisms underlying glycan recognition by plant PRRs remain limited.Currently,this knowledge is mainly focused on receptors of the LysM-PRR family,which are involved in the perception of various molecules,such as chitooligosaccharides from fungi and lipo-chitooligosaccharides(i.e.,Nod/MYC factors from bacteria and mycorrhiza,respectively)that trigger differential physiological responses.Nevertheless,additional families of plant PRRs have recently been implicated in oligosaccharide/polysaccharide recognition.These include receptor kinases(RKs)with leucine-rich repeat and Malectin domains in their ECDs(LRR-MAL RKs),Catharanthus roseus RECEPTOR-LIKE KINASE 1-LIKE group(CrRLK1L)with Malectin-like domains in their ECDs,as well as wall-associated kinases,lectin-RKs,and LRR-extensins.The characterization of structural basis of glycans recognition by these new plant receptors will shed light on their similarities with those of mammalians involved in glycan perception.The gained knowledge holds the potential to facilitate the development of sustainable,glycan-based crop protection solutions.
基金support from the National Natural Science Foundation of China(32302370 to P.W.)USDA NIFA(grant 2020-67013-31615 to P.H.).
文摘In plant immunity,a well-orchestrated cascade is initiated by the dimerization of receptor-like kinases(RLKs),followed by the phosphorylation of receptor-like cytoplasmic kinases(RLCKs)and subsequent activation of NADPH oxidases for ROS generation.Recent findings by Zhong et al.illustrated that a maize signaling module comprising ZmWAKLZmWIK-ZmBLK1-ZmRBOH4 governs quantitative disease resistance to grey leaf spot,a pervasive fungal disease in maize worldwide,unveiling the conservation of this signaling quartet in plant immunity.
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.
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The research leading to these results received funding from the European Research Council under the European Union Seventh Framework Pro-gramme ERC-2013-STG grant agreement 335691the Austrian Science Fund(FWF)P27818-B22,I 3033-B22+1 种基金the Austrian Academy of Sciences(OEAW)the Deutsche Forschungsgemeinschaft(DFG,German Research Foundation)under Germany’s Excellence Strategy-EXC 2070-390732324.
文摘In plants,the antagonism between growth and defense is hardwired by hormonal signaling.The perception of pathogen-associatedmolecularpatterns(PAMPs)frominvadingmicroorganismsinhibits auxin signalingand plant growth.Conversely,pathogens manipulate auxin signaling to promote disease,but how this hormone inhibits immunity is not fully understood.Ustilago maydis is a maize pathogen that induces auxin signaling in its host.We characterized a U.maydis effector protein,Naked1(Nkd1),that is translocated into the host nucleus.Through its native ethylene-responsive element binding factor-associated amphiphilic repression(EAR)motif,Nkd1 binds to the transcriptional co-repressors TOPLESS/TOPLESS-related(TPL/TPRs)and prevents the recruitment of a transcriptional repressor involved in hormonal signaling,leading to the derepression of auxin and jasmonate signaling and thereby promoting susceptibility to(hemi)biotrophic pathogens.A moderate upregulation of auxin signaling inhibits the PAMP-triggered reactive oxygen species(ROS)burst,an early defense response.Thus,our findings establish a clear mechanism for auxin-induced pathogen susceptibility.Engineered Nkd1 variants with increased expression or increased EAR-mediated TPL/TPR binding trigger typical salicylic-acid-mediated defense reactions,leading to pathogen resistance.This implies that moderate binding of Nkd1 to TPL is a result of a balancing evolutionary selection process to enable TPL manipulation while avoiding host recognition.
基金supported by National Science Foundation(NSF)(IOS-1951094)and National Institutes of Health(NIH)(R01GM092893)to P.H.,the Natural Science Foundation of Shandong Province(ZR2020MC022)and Youth Innovation Technology Project of Higher School in Shandong Province(2020KJF013)to S.H.The funding agencies have no roles in the design of the study and collection,analysis,and interpretation of data and in writing the manuscript.
文摘Plant plasma membrane-resident immune receptors regulate plant immunity by recognizing microbe-associated molecular patterns(MAMPs),damage-associated molecular patterns(DAMPs),and phytocytokines.Phytocytokines are plant endogenous peptides,which are usually produced in the cytosol and released into the apoplast when plant encounters pathogen infections.Phytocytokines regulate plant immunity through activating an overlapping signaling pathway with MAMPs/DAMPs with some unique features.Here,we highlight the current understanding of phytocytokine production,perception and functions in plant immunity,and discuss how plants and pathogens manipulate phytocytokine signaling for their own benefits during the plant-pathogen warfare.
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.
基金supported by the National Natural Science Foundation of China (grant no. 31671991 to FC)。
文摘Mitogen-activated protein kinase(MAPK) cascades play pivotal roles in plant defense against phytopathogens downstream of immune receptor complexes. The amplitude and duration of MAPK activation must be strictly controlled, but the underlying mechanism remains unclear. Here, we identified Arabidopsis CPL1(C-terminal domain phosphatase-like 1)as a negative regulator of microbe-associated molecular pattern(MAMP)-triggered immunity via a forward-genetic screen. Disruption of CPL1 significantly enhanced plant resistance to Pseudomonas pathogens induced by the bacterial peptide fg22. Furthermore, fg22-induced MPK3/MPK4/MPK6 phosphorylation was dramatically elevated in cpl1 mutants but severely impaired in CPL1 overexpression lines, suggesting that CPL1 might interfere with fg22-induced MAPK activation. Indeed, CPL1 directly interacted with MPK3 and MPK6, as well as the upstream MKK4 and MKK5. A firefy luciferase-based complementation assay indicated that the interaction between MKK4/MKK5 and MPK3/MPK6 was significantly reduced in the presence of CPL1. These results suggest that CPL1 plays a novel regulatory role in suppressing MAMP-induced MAPK cascade activation and MAMP-triggered immunity to bacterial pathogens.
