While SlPti5 has been shown to play a crucial role in the regulation of antagonistic genes in Solanum lycopersicum and Arabidopsis against pathogen infection,there have been no comprehensive studies on the effects of ...While SlPti5 has been shown to play a crucial role in the regulation of antagonistic genes in Solanum lycopersicum and Arabidopsis against pathogen infection,there have been no comprehensive studies on the effects of SlPti5 on the regulatory response mechanism of reactive oxygen species(ROS) system and hormone pathways during growth and disease resistance of tomato plants.Here,we investigated the function of SlPti5 in the defense response of tomato against Botrytis cinerea utilizing a virus-induced gene silencing(VIGS)-based system.Expression profile analysis showed that SlPti5 was significantly induced upon B.cinerea infection,with high expression levels in the leaves and fruit of tomato.VIGS-based silencing of SlPti5 inhibited early vegetative growth,increased the plant’s susceptibility to infection,promoted the development of ROS,affected the expression of genes involved in the ROS scavenging system,and attenuated the expression of genes associated with pathogenesis and the ethylene/jasmonic acid signaling pathways.In sum,our data demonstrated that SlPti5 stimulates the immune response of tomato plant to Botrytis cinerea infection by involving the ethylene(ET)-and jasmonic acid(JA)-mediated pathways and modulating the expression of some key pathogenesis-related(PR) genes.展开更多
In nature, plants constantly have to face pathogen attacks. However, plant disease rarely occurs due to efficient immune systems possessed by the host plants. Pathogens are perceived by two different recognition syste...In nature, plants constantly have to face pathogen attacks. However, plant disease rarely occurs due to efficient immune systems possessed by the host plants. Pathogens are perceived by two different recognition systems that initiate the so-called pattern-triggered immunity （PTI） and effector-triggered immunity （ETI）, both of which are accompanied by a set of induced defenses that usually repel pathogen attacks. Here we discuss the complex network of signaling pathways occurring during PTI, focusing on the involvement of mitogen-activated protein kinases.展开更多
Plant cells possess a two-layered immune system consisting of pattern-triggered immunity(PTI)and effector-triggered immunity(ETI), mediated by cell surface pattern-recognition receptors and intracellular nucleotide-bi...Plant cells possess a two-layered immune system consisting of pattern-triggered immunity(PTI)and effector-triggered immunity(ETI), mediated by cell surface pattern-recognition receptors and intracellular nucleotide-binding leucine-rich repeat receptors(NLRs), respectively. The CONSTITUTIVE EXPRESSION OF PR GENES 5(CPR5) nuclear pore complex protein negatively regulates ETI, including ETI-associated hypersensitive response. Here, we show that CPR5 is essential for the activation of various PTI responses in Arabidopsis, such as resistance to the non-adapted bacterium Pseudomonas syringae pv. tomato DC3000 hrc C-. In a forward-genetic screen for suppressors of cpr5, we identified the mediator protein MED4. Mutation of MED4 in cpr5 greatly restored the defective PTI of cpr5. Our findings reveal that CPR5 plays opposite roles in regulating PTI and ETI, and genetically regulates PTI via MED4.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
Rice blast, caused by the fungal pathogen Magnaporthe oryzae, is one of the most destructive diseases of rice worldwide. The rice-M, oryzae pathosystem has become a model in the study of plant-fungal interactions beca...Rice blast, caused by the fungal pathogen Magnaporthe oryzae, is one of the most destructive diseases of rice worldwide. The rice-M, oryzae pathosystem has become a model in the study of plant-fungal interactions because of its scientific advancement and economic importance. Recent studies have identified a number of new pathogen- associated molecular patterns （PAMPs） and effectors from the blast fungus that trigger rice immune responses upon perception. Interaction analyses between avirulence effectors and their cognate resistance proteins have provided new insights into the molecular basis of plant-fungal interactions. In this review, we summarize the recent research on the characterization of those genes in both M. oryzae and rice that are important for the PAMP- and effector-triggered immunity recognition and signaling processes. We also discuss future directions for research that will further our understanding of this pathosystem.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
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
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 innate immunity begins with the recognition of pathogens by plasma membrane localized pattern-recognition receptors(PRRs)and intracellular nucleotide-binding domain leucine-rich repeat containing receptors(NLRs)...Plant innate immunity begins with the recognition of pathogens by plasma membrane localized pattern-recognition receptors(PRRs)and intracellular nucleotide-binding domain leucine-rich repeat containing receptors(NLRs),which lead to pattern-triggered immunity(PTI)and effector-triggered immunity(ETI),respectively.For a long time,PTI and ETI have been regarded as two independent processes although they share multiple components and signal outputs.Increasing evidence shows an intimate link between PTI and ETI.PTI and ETI mutually potentiate each other,and this is essential for robust disease resistance during pathogen infection.An ancient class of NLRs called RNLs,so named because they carry a Resistance to Powdery Mildew 8(RPW8)-like coiled-coil(CC)domain in the N terminus,has emerged as a key node connecting PTI and ETI.RNLs not only act as helper NLRs that signal downstream of sensor NLRs,they also directly mediate PTI signaling by associating with PRR complexes.Here,we focus on Activated Disease Resistance 1(ADR1),a subclass of RNLs,and discuss its role and mechanism in plant immunity.展开更多
基金supported by the National Key Technology R&D Program of China (2016YFD0401201)the National Natural Science Foundation of China (31801602 and 31571897)+1 种基金the Project of Tianjin Education Commission Scientific Research Plan, China (2018KJ094)the National Science and Technology Major Project of China (2018ZX10101003-002-004)。
文摘While SlPti5 has been shown to play a crucial role in the regulation of antagonistic genes in Solanum lycopersicum and Arabidopsis against pathogen infection,there have been no comprehensive studies on the effects of SlPti5 on the regulatory response mechanism of reactive oxygen species(ROS) system and hormone pathways during growth and disease resistance of tomato plants.Here,we investigated the function of SlPti5 in the defense response of tomato against Botrytis cinerea utilizing a virus-induced gene silencing(VIGS)-based system.Expression profile analysis showed that SlPti5 was significantly induced upon B.cinerea infection,with high expression levels in the leaves and fruit of tomato.VIGS-based silencing of SlPti5 inhibited early vegetative growth,increased the plant’s susceptibility to infection,promoted the development of ROS,affected the expression of genes involved in the ROS scavenging system,and attenuated the expression of genes associated with pathogenesis and the ethylene/jasmonic acid signaling pathways.In sum,our data demonstrated that SlPti5 stimulates the immune response of tomato plant to Botrytis cinerea infection by involving the ethylene(ET)-and jasmonic acid(JA)-mediated pathways and modulating the expression of some key pathogenesis-related(PR) genes.
文摘In nature, plants constantly have to face pathogen attacks. However, plant disease rarely occurs due to efficient immune systems possessed by the host plants. Pathogens are perceived by two different recognition systems that initiate the so-called pattern-triggered immunity （PTI） and effector-triggered immunity （ETI）, both of which are accompanied by a set of induced defenses that usually repel pathogen attacks. Here we discuss the complex network of signaling pathways occurring during PTI, focusing on the involvement of mitogen-activated protein kinases.
基金supported by grants from the National Key R&D Program of China (2021YFA1300701)National Natural Science Foundation of China (32120103004, 32270282)the Hainan Excellent Talent Team, and the State Key Laboratory of Plant Genomics (SKLPG2016B-2)。
文摘Plant cells possess a two-layered immune system consisting of pattern-triggered immunity(PTI)and effector-triggered immunity(ETI), mediated by cell surface pattern-recognition receptors and intracellular nucleotide-binding leucine-rich repeat receptors(NLRs), respectively. The CONSTITUTIVE EXPRESSION OF PR GENES 5(CPR5) nuclear pore complex protein negatively regulates ETI, including ETI-associated hypersensitive response. Here, we show that CPR5 is essential for the activation of various PTI responses in Arabidopsis, such as resistance to the non-adapted bacterium Pseudomonas syringae pv. tomato DC3000 hrc C-. In a forward-genetic screen for suppressors of cpr5, we identified the mediator protein MED4. Mutation of MED4 in cpr5 greatly restored the defective PTI of cpr5. Our findings reveal that CPR5 plays opposite roles in regulating PTI and ETI, and genetically regulates PTI via MED4.
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.
基金This work was supported by the US NSF-IOS to G.L.W. （1120949）the National Natural Science Foundation of China to W.D.L. （31272034）+3 种基金 Y.S.N. （31101405） and X.L.W. （31101404） the 973 Project （2012CBl14005） of Ministry of Science and Technology China and the National Transgenic Crop Initiative to G.L.W. （2012ZX08009001） and the Scientific and Technological Innovation Program of Hunan Universities from Hunan Department of Science and Technology and the Program for Innovative Research Team in University from Ministry of Education in China IRT1239） to Z.L.W. No conflict of interest declared.
文摘Rice blast, caused by the fungal pathogen Magnaporthe oryzae, is one of the most destructive diseases of rice worldwide. The rice-M, oryzae pathosystem has become a model in the study of plant-fungal interactions because of its scientific advancement and economic importance. Recent studies have identified a number of new pathogen- associated molecular patterns （PAMPs） and effectors from the blast fungus that trigger rice immune responses upon perception. Interaction analyses between avirulence effectors and their cognate resistance proteins have provided new insights into the molecular basis of plant-fungal interactions. In this review, we summarize the recent research on the characterization of those genes in both M. oryzae and rice that are important for the PAMP- and effector-triggered immunity recognition and signaling processes. We also discuss future directions for research that will further our understanding of this pathosystem.
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.
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supported by the Postdoctoral Innovative Talent Support Program of China(BX2021355 to M.H.)the National Natural Science Foundation of China(31830019 and 31521001 to J.-M.Z.).
文摘Plant innate immunity begins with the recognition of pathogens by plasma membrane localized pattern-recognition receptors(PRRs)and intracellular nucleotide-binding domain leucine-rich repeat containing receptors(NLRs),which lead to pattern-triggered immunity(PTI)and effector-triggered immunity(ETI),respectively.For a long time,PTI and ETI have been regarded as two independent processes although they share multiple components and signal outputs.Increasing evidence shows an intimate link between PTI and ETI.PTI and ETI mutually potentiate each other,and this is essential for robust disease resistance during pathogen infection.An ancient class of NLRs called RNLs,so named because they carry a Resistance to Powdery Mildew 8(RPW8)-like coiled-coil(CC)domain in the N terminus,has emerged as a key node connecting PTI and ETI.RNLs not only act as helper NLRs that signal downstream of sensor NLRs,they also directly mediate PTI signaling by associating with PRR complexes.Here,we focus on Activated Disease Resistance 1(ADR1),a subclass of RNLs,and discuss its role and mechanism in plant immunity.
