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
The original online version of this article (Ghozlan, M.H., EL-Argawy, E., Tokgöz, S., Lakshman, D.K. and Mitra, A. (2020) Plant Defense against Necrotrophic Pathogens. American Journal of Plant Sciences, 11, 212...The original online version of this article (Ghozlan, M.H., EL-Argawy, E., Tokgöz, S., Lakshman, D.K. and Mitra, A. (2020) Plant Defense against Necrotrophic Pathogens. American Journal of Plant Sciences, 11, 2122-2138. https://doi.org/10.4236/ajps.2020.1112149) was published mistakenly without another co-author, Nikita Gambhir. In this regard, we revise authors and “how to cite” sections by adding her name.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
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
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
Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens,but this exposes the pathogen to potential recognition by the plant immune system.Therefore,the effector repertoire of a give...Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens,but this exposes the pathogen to potential recognition by the plant immune system.Therefore,the effector repertoire of a given pathogen must be balanced for a successful infection.Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors.One of these effectors,RipE1,is conserved in most R.solanacearum strains sequenced to date.In this work,we found that RipE1 triggers immunity in N.benthamiana,which requires the immune regulator SGT1,but not EDS1 or NRCs.Interestingly,RipE1-triggered immunity induces the accumulation of salicylic acid(SA)and the overexpression of several genes encoding phenylalanine-ammonia lyases(PALs),suggesting that the unconventional PALmediated pathway is responsible for the observed SA biosynthesis.Surprisingly,RipE1 recognition also induces the expression of jasmonic acid(JA)-responsive genes and JA biosynthesis,suggesting that both SA and JA may act cooperatively in response to RipE1.We further found that RipE1 expression leads to the accumulation of glutathione in plant cells,which precedes the activation of immune responses.R.solanacearum secretes another effector,RipAY,which is known to inhibit immune responses by degrading cellular glutathione.Accordingly,RipAY inhibits RipE1-triggered immune responses.This work shows a strategy employed by R.solanacearum to counteract the perception of its effector proteins by plant immune system.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
Necrotrophic pathogenic bacteria, fungi and oomycetes are widely distributed and are responsible for significant crop losses. Host plants deploy different defense mechanisms and appropriate immune responses to defend ...Necrotrophic pathogenic bacteria, fungi and oomycetes are widely distributed and are responsible for significant crop losses. Host plants deploy different defense mechanisms and appropriate immune responses to defend them against these pathogens. Regardless of the pathogen’s lifestyle, infection activates plant immune responses either through Pathogen/Microbe Associated Molecular Pattern (P/MAMP) or through Effector Triggered Immunity (ETI). However, as R-genes are not usually associated with resistance to necrotrophs, resistance is largely dependent on the balanced interplay between crucial phytohormones in complex signaling pathways involving jasmonic acid (JA), ethylene, salicylic acid (SA) and abscisic acid (ABA). An increase in salicylic acid levels enhances susceptibility to necrotrophic pathogens but promotes resistance to hemibiotrophs, whereas a deficiency in SA or SA signaling has either no significant impact or affects resistance only at the primary infection site. The same fashion is observed for JA signaling system that appears to elicit resistance against diseases caused by necrotrophic pathogens and can trigger systemic immunity conferring resistance against them. On the other hand, ABA can play a positive or negative role in plant defense responses to necrotrophs as ABA-mediated defense responses are dependent on specific plant-pathogen interactions. Understanding plant immune response against necrotrophic pathogens may lead to the development of resistant or tolerant crop cultivars.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
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
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 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.
文摘The original online version of this article (Ghozlan, M.H., EL-Argawy, E., Tokgöz, S., Lakshman, D.K. and Mitra, A. (2020) Plant Defense against Necrotrophic Pathogens. American Journal of Plant Sciences, 11, 2122-2138. https://doi.org/10.4236/ajps.2020.1112149) was published mistakenly without another co-author, Nikita Gambhir. In this regard, we revise authors and “how to cite” sections by adding her name.
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 the Strategic Priority Research Program of the Chinese Academy of Sciences(grant XDB27040204)the National Natural Science Foundation of China(grant 31571973)the Chinese 1000 Talents Program,and the Shanghai Center for Plant Stress Biology(Chinese Academy of Sciences).
文摘Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens,but this exposes the pathogen to potential recognition by the plant immune system.Therefore,the effector repertoire of a given pathogen must be balanced for a successful infection.Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors.One of these effectors,RipE1,is conserved in most R.solanacearum strains sequenced to date.In this work,we found that RipE1 triggers immunity in N.benthamiana,which requires the immune regulator SGT1,but not EDS1 or NRCs.Interestingly,RipE1-triggered immunity induces the accumulation of salicylic acid(SA)and the overexpression of several genes encoding phenylalanine-ammonia lyases(PALs),suggesting that the unconventional PALmediated pathway is responsible for the observed SA biosynthesis.Surprisingly,RipE1 recognition also induces the expression of jasmonic acid(JA)-responsive genes and JA biosynthesis,suggesting that both SA and JA may act cooperatively in response to RipE1.We further found that RipE1 expression leads to the accumulation of glutathione in plant cells,which precedes the activation of immune responses.R.solanacearum secretes another effector,RipAY,which is known to inhibit immune responses by degrading cellular glutathione.Accordingly,RipAY inhibits RipE1-triggered immune responses.This work shows a strategy employed by R.solanacearum to counteract the perception of its effector proteins by plant immune system.
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.
文摘Necrotrophic pathogenic bacteria, fungi and oomycetes are widely distributed and are responsible for significant crop losses. Host plants deploy different defense mechanisms and appropriate immune responses to defend them against these pathogens. Regardless of the pathogen’s lifestyle, infection activates plant immune responses either through Pathogen/Microbe Associated Molecular Pattern (P/MAMP) or through Effector Triggered Immunity (ETI). However, as R-genes are not usually associated with resistance to necrotrophs, resistance is largely dependent on the balanced interplay between crucial phytohormones in complex signaling pathways involving jasmonic acid (JA), ethylene, salicylic acid (SA) and abscisic acid (ABA). An increase in salicylic acid levels enhances susceptibility to necrotrophic pathogens but promotes resistance to hemibiotrophs, whereas a deficiency in SA or SA signaling has either no significant impact or affects resistance only at the primary infection site. The same fashion is observed for JA signaling system that appears to elicit resistance against diseases caused by necrotrophic pathogens and can trigger systemic immunity conferring resistance against them. On the other hand, ABA can play a positive or negative role in plant defense responses to necrotrophs as ABA-mediated defense responses are dependent on specific plant-pathogen interactions. Understanding plant immune response against necrotrophic pathogens may lead to the development of resistant or tolerant crop cultivars.
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 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.
