In nature,plants are under attack by a range of pathogens.To cope with these pathogens,plants have evolved a sophisticated immune system,including pattern-triggered immunity(PTI)initiated by pattern recognition recept...In nature,plants are under attack by a range of pathogens.To cope with these pathogens,plants have evolved a sophisticated immune system,including pattern-triggered immunity(PTI)initiated by pattern recognition receptors on the cell surface and effector-triggered immunity(ETI)activated by intracellular nucleotide-binding and leucine-rich repeat receptors.In recent years,increasing evidence has demonstrated that organelles such as the chloroplast play crucial roles in complete activation of plant immunity.In this review,we focus on the chloroplast and summarize its role in regulating the activation of immune events,including influx of calcium(Ca^(2+)),accumulation of reactive oxygen species(ROS),biosynthesis of phytohormones,and expression of defense-related genes.Because information exchange between the chloroplast and the nucleus is very important during plant immunity,we also highlight the importance of chloroplast-nucleus communication via stromules in plant immunity.This review reveals the function of the chloroplast in maintaining the trade-off between plant growth and immunity,and expands our understanding of how chloroplasts enable complete activation of plant immunity.展开更多
The SnRK2 gene family plays important roles in ABA mediated abiotic stress responses.However,the roles and functional mechanism of the SnRK2 gene family in plant immunity are largely unknown.In this study,we report th...The SnRK2 gene family plays important roles in ABA mediated abiotic stress responses.However,the roles and functional mechanism of the SnRK2 gene family in plant immunity are largely unknown.In this study,we report that OsSAPK10,a SnRK2 gene family protein in rice,positively regulates rice blast resistance.The ossapk10 mutation reduced rice blast resistance and overexpression of OsSAPK10 increased it.Furthermore,OsSAPK10 phosphorylates OsPAL1,a positive regulator of rice blast resistance,at Ser82 to stabilize it.Knocking out OsPAL1 also reduced rice blast resistance.Taken together,our findings revealed that OsSAPK10 positively regulates rice immunity via phosphorylating and stabilizing OsPAL1,providing new insight into the functional mechanism of the SnRK2 gene family in biotic stress responses.展开更多
Rice blast disease caused by Magnaporthe oryzae poses a serious threat to rice security worldwide.This filamentous pathogen modulates rice defense responses by secreting effectors to facilitate infection.The phytohorm...Rice blast disease caused by Magnaporthe oryzae poses a serious threat to rice security worldwide.This filamentous pathogen modulates rice defense responses by secreting effectors to facilitate infection.The phytohormone jasmonic acid(JA)plays crucial roles in the response to rice blast fungus.However,how M.oryzae disrupts JA-mediated resistance in rice is not well understood.In this study,we identify a new effector,a chloroplast-targeting protein(MoCHT1),from M.oryzae.Knocking out MoCHT1 decreases virulence,whereas heterologous expression of MoCHT1 in rice compromises disease resistance.MoCHT1 interacts with a rice LESION AND LAMINA BENDING(OsLLB)protein,a negative regulator of JA biosynthesis in the chloroplast.Loss-of-function of Os LLB leads to increased JA accumulation,thereby improving resistance to rice blast.The interaction between MoCHT1 and OsLLB results in the inhibition of OsLLB degradation,consequently reducing JA accumulation,thereby impairing JA content and decreasing plant disease resistance.Overall,this study reveals the molecular mechanism by which M.oryzae utilizes MoCHT1 to subvert rice JA signaling,broadening our understanding of how pathogens circumvent host immune responses by manipulating plant defense hormone biosynthesis.展开更多
Plants employ receptor-like kinases (RLKs)and receptor-like proteins for rapid recognition of invading pathogens,and RLKs then transmit signals to receptor-like cytoplasmic kinases (RLCKs)to activate immune responses....Plants employ receptor-like kinases (RLKs)and receptor-like proteins for rapid recognition of invading pathogens,and RLKs then transmit signals to receptor-like cytoplasmic kinases (RLCKs)to activate immune responses.RLKs are under fine regulation mediated by subcellular trafficking,which contributes to proper activation of plant immunity.In this study,we show that Arabidopsisthaliana RECEPTOR-LIKE KINASE 902 (RLK902)plays important roles in resistance to the bacterial pathogen Pseudomonas syringae, but not to the fungal powdery mildew pathogen Golovinomyces cichoracearum.RLK902 localizes at the plasma membrane and associates with ENHANCED DISEASE RESISTANCE 4 (EDR4),a protein involved in clathrin-mediated trafficking pathways.EDR4 and CLATHRIN HEAVY CHAIN 2 (CHC2)regulate the subcellular trafficking and accumulation of RLK902 protein.Furthermore,we found that RLKg02 directly associates with the RLCK BRASSINOSTEROID-SIGNALING KINASE1 (BSK1),a key component of plant immunity,but not with other members of the FLAGELLIN SENSING 2 immune complex.RLK902 phosphorylates BSK1,and its Ser-230 is a key phosphorylation site critical for RLK902-mediated defense signaling. Taken together,our data indicate that EDR4 regulates plant immunity by modulating the subcellular trafficking and protein accumulation of RLK902,and that RLK902 transmits immune signals by phosphorylating BSK1.展开更多
Mitogen-activated protein kinase(MAPK) cascades are highly conserved signaling modules that regulate plant immune responses. The Arabidopsis thaliana Raf-like MAPK kinase kinase ENHANCED DISEASE RESISTANCE1(EDR1) is a...Mitogen-activated protein kinase(MAPK) cascades are highly conserved signaling modules that regulate plant immune responses. The Arabidopsis thaliana Raf-like MAPK kinase kinase ENHANCED DISEASE RESISTANCE1(EDR1) is a key negative regulator of plant immunity that affects the protein levels of MKK4 and MKK5, two important MAPK cascade members, but the underlying mechanism is poorly understood. Here, genome-wide phosphorylation analysis demonstrated that the E3 ligase KEEP ON GOING(KEG) is phosphorylated in the edr1 mutant but not the wild type, suggesting that EDR1 negatively affects KEG phosphorylation. The identified phosphorylation sites in KEG appear to be important for its accumulation. The keg-4 mutant, a previously identified edr1 suppressor, enhances susceptibility to the powdery mildew pathogen Golovinomyces cichoracearum. In addition, MKK4 and MKK5 protein levels are reduced in the keg-4 mutant. Furthermore,we demonstrate that MKK4 and MKK5 associate with full-length KEG, but not with truncated KEG-RK or KEG-RKA, and that KEG ubiquitinates and mediates the degradation of MKK4 and MKK5. Taken together, these results indicate that MKK4 and MKK5 protein levels are regulated by KEG via ubiquitination, uncovering a mechanism by which plants finetune immune responses by regulating the homeostasis of key MAPK cascade members via ubiquitination and degradation.展开更多
Pattern recognition receptors(PRRs)sense ligands in pattern-triggered immunity(PTI).Plant PRRs include numerous receptor-like proteins(RLPs),but many RLPs remain functionally uncharacterized.Here,we examine an Arabido...Pattern recognition receptors(PRRs)sense ligands in pattern-triggered immunity(PTI).Plant PRRs include numerous receptor-like proteins(RLPs),but many RLPs remain functionally uncharacterized.Here,we examine an Arabidopsis thaliana RLP,RLP53,which positively regulates immune signaling.Our forward genetic screen for suppressors of enhanced disease resistance1(edr1)identified a point mutation in RLP53 that fully suppresses disease resistance and mildewinduced cell death in edr1 mutants.The rlp53 mutants showed enhanced susceptibility to virulent pathogens,including fungi,oomycetes,and bacteria,indicating that RLP53 is important for plant immunity.The ectodomain of RLP53 contains leucine-rich repeat(LRR)motifs.RLP53 constitutively associates with the LRR receptorlike kinase SUPPRESSOR OF BRASSINOSTEROIDINSENSITIVE1-ASSOCIATEDKINASE(BAK1)-INTERACTINGRECEPTORKINASE1(SOBIR1)and interacts with the co-receptor BAK1 in a pathogen-induced manner.The double mutation sobir1-12 bak1-5 suppresses edr1-mediated disease resistance,suggesting that EDR1 negatively regulates PTI modulated by the RLP53–SOBIR1–BAK1 complex.Moreover,the glycosylphosphatidylinositol(GPI)-anchored protein LORELEI-LIKE GPI-ANCHORED PROTEIN1(LLG1)interacts with RLP53 and mediates RLP53 accumulation in the plasma membrane.We thus uncovered the role of a novel RLP and its associated immune complex in plant defense responses and revealed a potential new mechanism underlying regulation of RLP immune function by a GPI-anchored protein.展开更多
Serotonin is ubiquitous across all forms of life and functions in responses to biotic and abiotic stresses.In rice,the conversion of tryptamine to serotonin is catalyzed by Sekiguchi lesion(SL).Previous studies have i...Serotonin is ubiquitous across all forms of life and functions in responses to biotic and abiotic stresses.In rice,the conversion of tryptamine to serotonin is catalyzed by Sekiguchi lesion(SL).Previous studies have identified an sl mutation(a null mutation of SL)in several rice varieties and confirmed its increase of resistance and cell death.However,a systematic understanding of the reprogrammed cellular processes causing cell death and resistance is lacking.We performed a multi-omics analysis to clarify the fundamental mechanisms at the protein,gene transcript,and metabolite levels.We found that cell death and Magnaporthe oryzae(M.oryzae)infection of the sl-MH-1 mutant activated plant hormone signal transduction involving salicylic acid(SA),jasmonic acid(JA),and abscisic acid(ABA)in multiple regulatory layers.We characterized the dynamic changes of several key hormone levels during disease progression and under the cell death conditions and showed that SA and JA positively regulated rice cell death and disease resistance.SL-overexpressing lines confirmed that the sl-MH-1 mutant positively regulated rice resistance to M.oryzae.Our studies shed light on cell death and facilitate further mechanistic dissection of programmed cell death in rice.展开更多
Receptor-like cytoplasmic kinase OsBSK1-2 was reported to play an important role in regulation of response to rice blast,but the signaling pathway remained unknown.In this study,we identified OsMAPKKK18 and previously...Receptor-like cytoplasmic kinase OsBSK1-2 was reported to play an important role in regulation of response to rice blast,but the signaling pathway remained unknown.In this study,we identified OsMAPKKK18 and previously uncharacterized MAPKKKs OsMAPKKK16 and OsMAPKKK19 that interact with OsBSK1-2.Expression of all three MAPKKKs was induced by Magnaporthe oryzae infection,and all three induced cell death when transiently expressed in Nicotiana benthamiana leaves.Knockout of OsMAPKKK16 and OsMAPKKK18 compromised blast resistance and overexpression of OsMAPKKK19 increased blast resistance,indicating that all three MAPKKKs are involved in regulation of rice blast response.Furthermore,both OsMAPKKK16 and OsMAPKKK19 interacted with and phosphorylated OsMKK4 and OsMKK5,and chitin-induced MAPK activation was suppressed in osmapkkk16 and osbsk1-2 mutants.OsMAPKKK18 was earlier reported to interact with and phosphorylate OsMKK4 and affect chitin-induced MAPK activation,suggesting that OsBSK1-2 is involved in regulation of immunity through multiple MAPK signaling pathways.Unlike BSK1 in Arabidopsis,OsBSK1-2 was not involved in response to avirulent M.oryzae strains.Taken together,our results revealed important roles of OsMAPKKK16/18/19 and a OsBSK1-2-OsMAPKKK16/18/19-OsMKK4/5 module in regulating response to rice blast.展开更多
Gray blight disease(GBD)causes significant losses in tea production in China.Although genes and biological processes involved in resistance to fungal disease in tea plants have been identified,specific mechanisms of t...Gray blight disease(GBD)causes significant losses in tea production in China.Although genes and biological processes involved in resistance to fungal disease in tea plants have been identified,specific mechanisms of the GBD infection process remain unknown.In this study,morphological and multi-gene(TEF-TUB-ITS)phylogenetic characteristics were used to identify isolate CLBB1 of Pseudopestalotiopsis vietnamensis.Pathogenicity tests confirmed that isolate CLBB1 from tea leaves caused GBD in the susceptible tea cultivar Wuyi Rock(Camellia sinensis var.sinensis cv.Shuixian).Spores began to germinate 24 h after infection(hai),and after 48 h,elongated fungal hyphae formed from a single conidium.Transcriptome analysis revealed that 482,517,and 369 genes were differentially expressed at 24,48,and 72 hai,respectively,in Wuyi Rock tea leaves.Isolate CLBB1 infection elicited phenotype-related responses and activated defense-related pathways,including plant–pathogen interaction,MAPK signaling,and plant hormone signal transduction,suggesting a possible mechanism underlying phenotype-based susceptibility to CLBB1.Thus,a new Ps.vietnamensis strain causing GBD in the tea cultivar‘Shuixian’was discovered in this study.Transcriptome analysis indicated that pathogen invasion activated chitin-related MAPK pathways and that tea plants required a hormone to restrict CLBB1.展开更多
Pattern-triggered immunity(PTI)includes the different transcriptional and physiological responses that enable plants to ward off microbial invasion.Surface-localized pattern-recognition receptors(PRRs)recognize conser...Pattern-triggered immunity(PTI)includes the different transcriptional and physiological responses that enable plants to ward off microbial invasion.Surface-localized pattern-recognition receptors(PRRs)recognize conserved microbeassociated molecular patterns(MAMPs)and initiate a branched signaling cascade that culminate in an effective restriction of pathogen growth.In the model species Arabidopsis thaliana,early PTI events triggered by different PRRs are broadly conserved although their nature or intensity is dependent on the origin and features of the detected MAMP.In order to provide a functional basis for disease resistance in leafy vegetable crops,we surveyed the conservation of PTI events in Brassica rapa ssp.pekinensis.We identified the PRR homologs present in B.rapa genome and found that only one of the two copies of the bacterial Elongation factor-Tu receptor(EFR)might function.We also characterized the extent and unexpected specificity of the transcriptional changes occurring when B.rapa seedlings are treated with two unrelated MAMPs,the bacterial flagellin flg22 peptide and the fungal cell wall component chitin.Finally,using a MAMP-induced protection assay,we could show that bacterial and fungal MAMPs elicit a robust immunity in B.rapa,despite significant differences in the kinetic and amplitude of the early signaling events.Our data support the relevance of PTI for crop protection and highlight specific functional target for disease resistance breeding in Brassica crops.展开更多
Plants encounter numerous microorganisms in the environment.However,only a few microbes are pathogenic to a plant species.To colonize plants,pathogens should be able to bypass or suppress multiple layers of the plant ...Plants encounter numerous microorganisms in the environment.However,only a few microbes are pathogenic to a plant species.To colonize plants,pathogens should be able to bypass or suppress multiple layers of the plant defense system,composed of pre-formed physico-chemical barriers and post-invasive immune systems.Thus,each plant pathogenic microorganism has its own host range,depending on the direction in which it is specialized or adapted.But,simultaneously,this specialization results in a lack of adaptation to most other plants,which have different immune components compared to the host plant species of a given pathogen.展开更多
Phytopathogens,such as the rice blast fungus Magnaporthe oryzae,suppress plant immunity for reproduction by secreting effectors into plant cells.The M.oryzae effector AvrPib is known to be recognized by Pib,an intrace...Phytopathogens,such as the rice blast fungus Magnaporthe oryzae,suppress plant immunity for reproduction by secreting effectors into plant cells.The M.oryzae effector AvrPib is known to be recognized by Pib,an intracellular nucleotide-binding,leucine-rich repeat receptor(NLR),in rice.However,how AvrPib manipulates blast resistance and its potential targets in rice remains unclear.In this study,we showed that AvrPib interacts with the rice MAP KINASE KINASE KINASE 72(OsMAPKKK72),a previously uncharacterized Raf-like MAPKKK.The osmapkkk72 mutant shows enhanced susceptibility to the M.oryzae strain Guy11 and reduced mitogen-activated protein kinase(MAPK)activation after treatment with chitin.Furthermore,OsMAPKKK72 interacts with MAP KINASE KINASE 9(OsMKK9)and increases the interaction between OsMKK9 and OsMPK3/6.Accordingly,OsMKK9 positively regulates rice blast resistance and increases MAPK activation in an OsMAPKKK72-dependent manner following chitin treatment in rice,suggesting that OsMAPKKK72 may serve as a scaffold in the MAPK cascade.AvrPib inhibits the interaction between OsMAPKKK72 and OsMKK9,leading to reduced MAPK activation,which is mediated by OsMKK9.Taken together,our results reveal the critical roles of OsMAPKKK72 in blast resistance and uncover a mechanism wherein AvrPib suppresses rice blast resistance by interference with MAPK activation by targeting a key component in the MAPK cascade.展开更多
Plants have evolved multiple defense strategies to cope with pathogens, among which plant immune signaling that relies on cell-surface localized and intracellular receptors takes fundamental roles. Exciting breakthrou...Plants have evolved multiple defense strategies to cope with pathogens, among which plant immune signaling that relies on cell-surface localized and intracellular receptors takes fundamental roles. Exciting breakthroughs were made recently on the signaling mechanisms of pattern recognition receptors(PRRs) and intracellular nucleotide-binding site(NBS) and leucine-rich repeat(LRR)domain receptors(NLRs). This review summarizes the current view of PRRs activation, emphasizing the most recent discoveries about PRRs’ dynamic regulation and signaling mechanisms directly leading to downstream molecular events including mitogen-activated protein kinase(MAPK) activation and calcium(Ca2+) burst. Plants also have evolved intracellular NLRs to perceive the presence of specific pathogen effectors and trigger more robust immune responses. We also discuss the current understanding of the mechanisms of NLR activation, which has been greatly advanced by recent breakthroughs including structures of the first full-length plant NLR complex, findings of NLR sensor-helper pairs and novel biochemical activity of Toll/interleukin-1 receptor(TIR) domain.展开更多
In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disea...In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.展开更多
Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The ...Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The Arabidopsis NLR protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) forms a precomplex with HOPZ-ETI-DEFICIENT 1 (ZED1),a receptor-like cytoplasmic kinase (RLCK) XII-2 subfamily member, to recognize the Pseudomonas syringae effector HopZ1 a. We previously described a dominant mutant of Arabi-dopsis ZED1, zed1-D, which displays temperature-sensitive autoimmunity in a ZAR1-dependent manner. Here, we report that the RLCKs SUPPRESSOR OF ZED1-D1 (SZE1) and SZE2 associate with the ZAR1-ZED1 complex and are required for the ZED7-D-activated autoimmune response and HopZ1a-triggered immunity. We show that SZE1 but not SZE2 has autophosphorylation activity, and that the N-terminal myristoylation of both SZE1 and SZE2 is critical for their plasma membrane localization and ZED1-D-activated autoimmunity. Furthermore, we demonstrate that SZE1 and SZE2 both interact with ZAR1 to form ja functional complex and are required for resistance against P. syringae pv. tomato DC3000 ex-pressing HopZIa. We also provide evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1, leading to its activation. Taken together, our re-sults reveal SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity.展开更多
Life or death?It’s a question animal and plant cells ask themselves during development and throughout their lives–and when they choose the latter option,cells can execute a genetically programmed set of cellular fun...Life or death?It’s a question animal and plant cells ask themselves during development and throughout their lives–and when they choose the latter option,cells can execute a genetically programmed set of cellular functions that result in cell death.In animals and plants,the execution of programmed cell death is critical for proper development and for immunity against invading microbes.展开更多
Plants need to fine-tune defense responses to maintain a robust but flexible host barrier to various pathogens.Helix-loop-helix/basic helix-loop-helix(HLH/bHLH)complexes play important roles in fine-tuning plant devel...Plants need to fine-tune defense responses to maintain a robust but flexible host barrier to various pathogens.Helix-loop-helix/basic helix-loop-helix(HLH/bHLH)complexes play important roles in fine-tuning plant development.However,the function of these genes in plant immunity and how they are regulated remain obscure.Here,we identified an atypical bHLH transcription factor,Oryza sativa(Os)HLH46,that interacts with rice receptor-like cytoplasmic kinase(RLCK)Os BRASSINOSTEROID-SIGNALING KINASE1-2(OsBSK1-2),which plays a key role in rice blast resistance.OsBSK1-2 stabilized OsHLH46 both in vivo and in vitro.In addition,OsHLH46 positively regulates rice blast resistance,which depends on OsBSK1-2.OsHLH46 has no transcriptional activation activity and interacts with a typical bHLH protein,OsbHLH6,which negatively regulates rice blast resistance.OsbHLH6 binds to the promoter of OsWRKY45 and inhibits its expression,while OsHLH46 suppresses the function of OsbHLH6 by blocking its DNA binding and transcriptional inhibition of OsWRKY45.Consistent with these findings,OsWRKY45 was up-regulated in OsHLH46-overexpressing plants.In addition,the oshlh46 mutant overexpressing OsbHLH6 is more susceptible to Magnaporthe oryzae than is the wild type,suggesting that OsHLH46 suppresses OsbHLH6-mediated rice blast resistance.Our results not only demonstrated that OsBSK1-2 regulates rice blast resistance via the OsHLH46/OsbHLH6 complex,but also uncovered a new mechanism for plants to fine-tune plant immunity by regulating the HLH/bHLH complex via RLCKs.展开更多
Mitogen-activated protein kinase(MAPK)activation is one of the significant immune events that respond to pathogens in plants.A MAPK cascade often contains a MAPK kinase kinase(MAPKKK),a MAPK kinase(MAPKK/MKK),and a MA...Mitogen-activated protein kinase(MAPK)activation is one of the significant immune events that respond to pathogens in plants.A MAPK cascade often contains a MAPK kinase kinase(MAPKKK),a MAPK kinase(MAPKK/MKK),and a MAPK.The well-characterized MAPK cascade,to date,is the MAPKKK3/4/5-MKK4/5-MPK3/6 module.Soybean cyst nematodes(SCN)is one of the most devastating soybean pathogens.However,the early immune components contributing to soybean resistance to SCN and the role of the MAPK cascade in the soybean-SCN interaction remain unclear.A recent study published in Plant Cell discovered that GmMPK3/6 phosphorylates a receptor-like cytoplasmic kinase(RLCK),CDG1-LIKE1(GmCDL1),and maintains the stability of GmCDL1 in soybean.Remarkably,GmCDL1 enhances GmMPK3/6 activation and resistance to SCN by phosphorylating GmMAPKKK5 and activating the GmMAPKKK5-GmMKK4-GmMPK3/6 cascade.In addition,two L-type lectin receptor kinases(LecRKs),GmLecRK02g and GmLecRK08g,are involved in the GmCDL1 function after the perception of SCN.taken together,this study not only discovers a complete early immune pathway that responds to SCN infection in soybean,but also reveals a molecular mechanism by which plants maintain the activation of the MAPK cascade and resistance.展开更多
Plants possess effective immune systems that defend against most microbial attackers.Recent plant immunity research has focused on the classic binary defense model involving the pivotal role of small-molecule hormones...Plants possess effective immune systems that defend against most microbial attackers.Recent plant immunity research has focused on the classic binary defense model involving the pivotal role of small-molecule hormones in regulating the plant defense signaling network.Although most of our current understanding comes from studies that relied on information derived from a limited number of pathosystems,newer studies concerning the incredibly diverse interactions between plants and microbes are providing additional insights into other novel mechanisms.Here,we review the roles of both classical and more recently identified components of defense signaling pathways and stress hormones in regulating the ambivalence effect during responses to diverse pathogens.Because of their different lifestyles,effective defense against biotrophic pathogens normally leads to increased susceptibility to necrotrophs,and vice versa.Given these opposing forces,the plant potentially faces a trade-off when it mounts resistance to a specific pathogen,a phenomenon referred to here as the ambivalence effect.We also highlight a novel mechanism by which translational control of the proteins involved in the ambivalence effect can be used to engineer durable and broad-spectrum disease resistance,regardless of the lifestyle of the invading pathogen.展开更多
Triticeae species,including wheat,barley,and rye,are critical for global food security.Mapping agronomically important genes is crucial for elucidating molecular mechanisms and improving crops.However,Triticeae includ...Triticeae species,including wheat,barley,and rye,are critical for global food security.Mapping agronomically important genes is crucial for elucidating molecular mechanisms and improving crops.However,Triticeae includes many wild relatives with desirable agronomic traits,and frequent introgressions occurred during Triticeae evolution and domestication.Thus,Triticeae genomes are generally large and complex,making the localization of genes or functional elements that control agronomic traits challenging.Here,we developed Triti-Map,which contains a suite of user-friendly computational packages specifically designed and optimized to overcome the obstacles of gene mapping in Triticeae,as well as a web interface integrating multi-omics data from Triticeae for the efficient mining of genes or functional elements that control particular traits.The Triti-Map pipeline accepts bothDNA and RNAbulk-segregated sequencing data as well as traditional QTL data as inputs for locating genes and elucidating their functions.We illustrate the usage of Triti-Map with a combination of bulk-segregated ChIP-seq data to detect a wheat disease-resistance gene with its promoter sequence that is absent from the reference genome and clarify its evolutionary process.We hope that Triti-Map will facilitate gene isolation and accelerate Triticeae breeding.展开更多
基金supported by grants from the Natural Science Foundation of Fujian Province,China(grant no.2024J09022)the National Natural Science Foundation of China(grant no.32370302)the Open Fund of Fujian Provincial Key Laboratory of Eco-Industrial Green Technology(grant no.WYKF-EIGT2022-6).
文摘In nature,plants are under attack by a range of pathogens.To cope with these pathogens,plants have evolved a sophisticated immune system,including pattern-triggered immunity(PTI)initiated by pattern recognition receptors on the cell surface and effector-triggered immunity(ETI)activated by intracellular nucleotide-binding and leucine-rich repeat receptors.In recent years,increasing evidence has demonstrated that organelles such as the chloroplast play crucial roles in complete activation of plant immunity.In this review,we focus on the chloroplast and summarize its role in regulating the activation of immune events,including influx of calcium(Ca^(2+)),accumulation of reactive oxygen species(ROS),biosynthesis of phytohormones,and expression of defense-related genes.Because information exchange between the chloroplast and the nucleus is very important during plant immunity,we also highlight the importance of chloroplast-nucleus communication via stromules in plant immunity.This review reveals the function of the chloroplast in maintaining the trade-off between plant growth and immunity,and expands our understanding of how chloroplasts enable complete activation of plant immunity.
基金supported by National Key Research and Development Program of China(2023YFF1000500)the National Natural Science Foundation of China(32161133012).
文摘The SnRK2 gene family plays important roles in ABA mediated abiotic stress responses.However,the roles and functional mechanism of the SnRK2 gene family in plant immunity are largely unknown.In this study,we report that OsSAPK10,a SnRK2 gene family protein in rice,positively regulates rice blast resistance.The ossapk10 mutation reduced rice blast resistance and overexpression of OsSAPK10 increased it.Furthermore,OsSAPK10 phosphorylates OsPAL1,a positive regulator of rice blast resistance,at Ser82 to stabilize it.Knocking out OsPAL1 also reduced rice blast resistance.Taken together,our findings revealed that OsSAPK10 positively regulates rice immunity via phosphorylating and stabilizing OsPAL1,providing new insight into the functional mechanism of the SnRK2 gene family in biotic stress responses.
基金funded by the Biological Breeding-National Science and Technology Major Projects(2023ZD04070)the National Natural Science Foundation of China(31970284,31900385)+1 种基金the Fujian Provincial Science and Technology Key Project(2022NZ030014)the Natural Science Foundation of Fujian Province,China(2023J01483,2022J01616)。
文摘Rice blast disease caused by Magnaporthe oryzae poses a serious threat to rice security worldwide.This filamentous pathogen modulates rice defense responses by secreting effectors to facilitate infection.The phytohormone jasmonic acid(JA)plays crucial roles in the response to rice blast fungus.However,how M.oryzae disrupts JA-mediated resistance in rice is not well understood.In this study,we identify a new effector,a chloroplast-targeting protein(MoCHT1),from M.oryzae.Knocking out MoCHT1 decreases virulence,whereas heterologous expression of MoCHT1 in rice compromises disease resistance.MoCHT1 interacts with a rice LESION AND LAMINA BENDING(OsLLB)protein,a negative regulator of JA biosynthesis in the chloroplast.Loss-of-function of Os LLB leads to increased JA accumulation,thereby improving resistance to rice blast.The interaction between MoCHT1 and OsLLB results in the inhibition of OsLLB degradation,consequently reducing JA accumulation,thereby impairing JA content and decreasing plant disease resistance.Overall,this study reveals the molecular mechanism by which M.oryzae utilizes MoCHT1 to subvert rice JA signaling,broadening our understanding of how pathogens circumvent host immune responses by manipulating plant defense hormone biosynthesis.
文摘Plants employ receptor-like kinases (RLKs)and receptor-like proteins for rapid recognition of invading pathogens,and RLKs then transmit signals to receptor-like cytoplasmic kinases (RLCKs)to activate immune responses.RLKs are under fine regulation mediated by subcellular trafficking,which contributes to proper activation of plant immunity.In this study,we show that Arabidopsisthaliana RECEPTOR-LIKE KINASE 902 (RLK902)plays important roles in resistance to the bacterial pathogen Pseudomonas syringae, but not to the fungal powdery mildew pathogen Golovinomyces cichoracearum.RLK902 localizes at the plasma membrane and associates with ENHANCED DISEASE RESISTANCE 4 (EDR4),a protein involved in clathrin-mediated trafficking pathways.EDR4 and CLATHRIN HEAVY CHAIN 2 (CHC2)regulate the subcellular trafficking and accumulation of RLK902 protein.Furthermore,we found that RLKg02 directly associates with the RLCK BRASSINOSTEROID-SIGNALING KINASE1 (BSK1),a key component of plant immunity,but not with other members of the FLAGELLIN SENSING 2 immune complex.RLK902 phosphorylates BSK1,and its Ser-230 is a key phosphorylation site critical for RLK902-mediated defense signaling. Taken together,our data indicate that EDR4 regulates plant immunity by modulating the subcellular trafficking and protein accumulation of RLK902,and that RLK902 transmits immune signals by phosphorylating BSK1.
基金supported by grants from the National Natural Science Foundation of China (31761133017 and 31525019) to D.T。
文摘Mitogen-activated protein kinase(MAPK) cascades are highly conserved signaling modules that regulate plant immune responses. The Arabidopsis thaliana Raf-like MAPK kinase kinase ENHANCED DISEASE RESISTANCE1(EDR1) is a key negative regulator of plant immunity that affects the protein levels of MKK4 and MKK5, two important MAPK cascade members, but the underlying mechanism is poorly understood. Here, genome-wide phosphorylation analysis demonstrated that the E3 ligase KEEP ON GOING(KEG) is phosphorylated in the edr1 mutant but not the wild type, suggesting that EDR1 negatively affects KEG phosphorylation. The identified phosphorylation sites in KEG appear to be important for its accumulation. The keg-4 mutant, a previously identified edr1 suppressor, enhances susceptibility to the powdery mildew pathogen Golovinomyces cichoracearum. In addition, MKK4 and MKK5 protein levels are reduced in the keg-4 mutant. Furthermore,we demonstrate that MKK4 and MKK5 associate with full-length KEG, but not with truncated KEG-RK or KEG-RKA, and that KEG ubiquitinates and mediates the degradation of MKK4 and MKK5. Taken together, these results indicate that MKK4 and MKK5 protein levels are regulated by KEG via ubiquitination, uncovering a mechanism by which plants finetune immune responses by regulating the homeostasis of key MAPK cascade members via ubiquitination and degradation.
基金supported by grants from the National Natural Science Foundation of China(32161133012 and 31830077)to D.T.
文摘Pattern recognition receptors(PRRs)sense ligands in pattern-triggered immunity(PTI).Plant PRRs include numerous receptor-like proteins(RLPs),but many RLPs remain functionally uncharacterized.Here,we examine an Arabidopsis thaliana RLP,RLP53,which positively regulates immune signaling.Our forward genetic screen for suppressors of enhanced disease resistance1(edr1)identified a point mutation in RLP53 that fully suppresses disease resistance and mildewinduced cell death in edr1 mutants.The rlp53 mutants showed enhanced susceptibility to virulent pathogens,including fungi,oomycetes,and bacteria,indicating that RLP53 is important for plant immunity.The ectodomain of RLP53 contains leucine-rich repeat(LRR)motifs.RLP53 constitutively associates with the LRR receptorlike kinase SUPPRESSOR OF BRASSINOSTEROIDINSENSITIVE1-ASSOCIATEDKINASE(BAK1)-INTERACTINGRECEPTORKINASE1(SOBIR1)and interacts with the co-receptor BAK1 in a pathogen-induced manner.The double mutation sobir1-12 bak1-5 suppresses edr1-mediated disease resistance,suggesting that EDR1 negatively regulates PTI modulated by the RLP53–SOBIR1–BAK1 complex.Moreover,the glycosylphosphatidylinositol(GPI)-anchored protein LORELEI-LIKE GPI-ANCHORED PROTEIN1(LLG1)interacts with RLP53 and mediates RLP53 accumulation in the plasma membrane.We thus uncovered the role of a novel RLP and its associated immune complex in plant defense responses and revealed a potential new mechanism underlying regulation of RLP immune function by a GPI-anchored protein.
基金supported by the Collaborative Innovation Engineering“5511”(XTCXGC2021002)the National Natural Science Foundation of China(U1805232)+1 种基金the Youth Program of National Natural Science Foundation of China(31301654)the Youth Program of Fujian Academy of Agricultural Sciences(YC2019004)。
文摘Serotonin is ubiquitous across all forms of life and functions in responses to biotic and abiotic stresses.In rice,the conversion of tryptamine to serotonin is catalyzed by Sekiguchi lesion(SL).Previous studies have identified an sl mutation(a null mutation of SL)in several rice varieties and confirmed its increase of resistance and cell death.However,a systematic understanding of the reprogrammed cellular processes causing cell death and resistance is lacking.We performed a multi-omics analysis to clarify the fundamental mechanisms at the protein,gene transcript,and metabolite levels.We found that cell death and Magnaporthe oryzae(M.oryzae)infection of the sl-MH-1 mutant activated plant hormone signal transduction involving salicylic acid(SA),jasmonic acid(JA),and abscisic acid(ABA)in multiple regulatory layers.We characterized the dynamic changes of several key hormone levels during disease progression and under the cell death conditions and showed that SA and JA positively regulated rice cell death and disease resistance.SL-overexpressing lines confirmed that the sl-MH-1 mutant positively regulated rice resistance to M.oryzae.Our studies shed light on cell death and facilitate further mechanistic dissection of programmed cell death in rice.
基金This work was supported by the National Key Research and Development Program of China(2022YFF1001500)Key Program of Technology and Science in Fujian province(2020NZ08016).
文摘Receptor-like cytoplasmic kinase OsBSK1-2 was reported to play an important role in regulation of response to rice blast,but the signaling pathway remained unknown.In this study,we identified OsMAPKKK18 and previously uncharacterized MAPKKKs OsMAPKKK16 and OsMAPKKK19 that interact with OsBSK1-2.Expression of all three MAPKKKs was induced by Magnaporthe oryzae infection,and all three induced cell death when transiently expressed in Nicotiana benthamiana leaves.Knockout of OsMAPKKK16 and OsMAPKKK18 compromised blast resistance and overexpression of OsMAPKKK19 increased blast resistance,indicating that all three MAPKKKs are involved in regulation of rice blast response.Furthermore,both OsMAPKKK16 and OsMAPKKK19 interacted with and phosphorylated OsMKK4 and OsMKK5,and chitin-induced MAPK activation was suppressed in osmapkkk16 and osbsk1-2 mutants.OsMAPKKK18 was earlier reported to interact with and phosphorylate OsMKK4 and affect chitin-induced MAPK activation,suggesting that OsBSK1-2 is involved in regulation of immunity through multiple MAPK signaling pathways.Unlike BSK1 in Arabidopsis,OsBSK1-2 was not involved in response to avirulent M.oryzae strains.Taken together,our results revealed important roles of OsMAPKKK16/18/19 and a OsBSK1-2-OsMAPKKK16/18/19-OsMKK4/5 module in regulating response to rice blast.
基金supported by the Central Special Project for Fujian Local Science and Technology Development(2020L3025)the Fujian Natural Science Foundation(2020J01410)+4 种基金a Fujian Education and Scientific Research Project(JAT190789)the Talent-Recruiting Program of Wuyi University(YJ201503)the Open Fund of Fujian Provincial Key Laboratory of Eco-Industrial Green Technology(WYKF2019-2)a Chongqing Natural Science Foundation Project(cstc2021jcyj-msxmX0322)the Scientific and Technological Research Program of Chongqing Municipal Education Commission(KJQN202101246).
文摘Gray blight disease(GBD)causes significant losses in tea production in China.Although genes and biological processes involved in resistance to fungal disease in tea plants have been identified,specific mechanisms of the GBD infection process remain unknown.In this study,morphological and multi-gene(TEF-TUB-ITS)phylogenetic characteristics were used to identify isolate CLBB1 of Pseudopestalotiopsis vietnamensis.Pathogenicity tests confirmed that isolate CLBB1 from tea leaves caused GBD in the susceptible tea cultivar Wuyi Rock(Camellia sinensis var.sinensis cv.Shuixian).Spores began to germinate 24 h after infection(hai),and after 48 h,elongated fungal hyphae formed from a single conidium.Transcriptome analysis revealed that 482,517,and 369 genes were differentially expressed at 24,48,and 72 hai,respectively,in Wuyi Rock tea leaves.Isolate CLBB1 infection elicited phenotype-related responses and activated defense-related pathways,including plant–pathogen interaction,MAPK signaling,and plant hormone signal transduction,suggesting a possible mechanism underlying phenotype-based susceptibility to CLBB1.Thus,a new Ps.vietnamensis strain causing GBD in the tea cultivar‘Shuixian’was discovered in this study.Transcriptome analysis indicated that pathogen invasion activated chitin-related MAPK pathways and that tea plants required a hormone to restrict CLBB1.
基金the support National Research Foundation of Korea(NRF)funded by the Ministry of Education(Projects No.2017R1D1A1B03035487 and No.2019R1I1A1A01060721,Basic Science Research Program and Project No.2018R1A5A1023599,SRC).C.S.was supported by the Creative-Pioneering Researchers Program through Seoul National University.
文摘Pattern-triggered immunity(PTI)includes the different transcriptional and physiological responses that enable plants to ward off microbial invasion.Surface-localized pattern-recognition receptors(PRRs)recognize conserved microbeassociated molecular patterns(MAMPs)and initiate a branched signaling cascade that culminate in an effective restriction of pathogen growth.In the model species Arabidopsis thaliana,early PTI events triggered by different PRRs are broadly conserved although their nature or intensity is dependent on the origin and features of the detected MAMP.In order to provide a functional basis for disease resistance in leafy vegetable crops,we surveyed the conservation of PTI events in Brassica rapa ssp.pekinensis.We identified the PRR homologs present in B.rapa genome and found that only one of the two copies of the bacterial Elongation factor-Tu receptor(EFR)might function.We also characterized the extent and unexpected specificity of the transcriptional changes occurring when B.rapa seedlings are treated with two unrelated MAMPs,the bacterial flagellin flg22 peptide and the fungal cell wall component chitin.Finally,using a MAMP-induced protection assay,we could show that bacterial and fungal MAMPs elicit a robust immunity in B.rapa,despite significant differences in the kinetic and amplitude of the early signaling events.Our data support the relevance of PTI for crop protection and highlight specific functional target for disease resistance breeding in Brassica crops.
基金supported by the National Research Foundation of Korea funded by the Korean government(MSIT)(NRF-RS-2025-00512558NRF-RS-2024-00333777 to D.C.and NRF-RS-2024-00333225 to S.O.).
文摘Plants encounter numerous microorganisms in the environment.However,only a few microbes are pathogenic to a plant species.To colonize plants,pathogens should be able to bypass or suppress multiple layers of the plant defense system,composed of pre-formed physico-chemical barriers and post-invasive immune systems.Thus,each plant pathogenic microorganism has its own host range,depending on the direction in which it is specialized or adapted.But,simultaneously,this specialization results in a lack of adaptation to most other plants,which have different immune components compared to the host plant species of a given pathogen.
基金supported by grants from the Biological Breeding-National Science and Technology Major Projects(2023ZD04070)the National Natural Science Foundation of China(32370302)the Natural Science Foundation of Fujian Province,China(2024J09022)。
文摘Phytopathogens,such as the rice blast fungus Magnaporthe oryzae,suppress plant immunity for reproduction by secreting effectors into plant cells.The M.oryzae effector AvrPib is known to be recognized by Pib,an intracellular nucleotide-binding,leucine-rich repeat receptor(NLR),in rice.However,how AvrPib manipulates blast resistance and its potential targets in rice remains unclear.In this study,we showed that AvrPib interacts with the rice MAP KINASE KINASE KINASE 72(OsMAPKKK72),a previously uncharacterized Raf-like MAPKKK.The osmapkkk72 mutant shows enhanced susceptibility to the M.oryzae strain Guy11 and reduced mitogen-activated protein kinase(MAPK)activation after treatment with chitin.Furthermore,OsMAPKKK72 interacts with MAP KINASE KINASE 9(OsMKK9)and increases the interaction between OsMKK9 and OsMPK3/6.Accordingly,OsMKK9 positively regulates rice blast resistance and increases MAPK activation in an OsMAPKKK72-dependent manner following chitin treatment in rice,suggesting that OsMAPKKK72 may serve as a scaffold in the MAPK cascade.AvrPib inhibits the interaction between OsMAPKKK72 and OsMKK9,leading to reduced MAPK activation,which is mediated by OsMKK9.Taken together,our results reveal the critical roles of OsMAPKKK72 in blast resistance and uncover a mechanism wherein AvrPib suppresses rice blast resistance by interference with MAPK activation by targeting a key component in the MAPK cascade.
基金supported by grant from the National Natural Science Foundation of China (31830077 and 31761133017) to D.T
文摘Plants have evolved multiple defense strategies to cope with pathogens, among which plant immune signaling that relies on cell-surface localized and intracellular receptors takes fundamental roles. Exciting breakthroughs were made recently on the signaling mechanisms of pattern recognition receptors(PRRs) and intracellular nucleotide-binding site(NBS) and leucine-rich repeat(LRR)domain receptors(NLRs). This review summarizes the current view of PRRs activation, emphasizing the most recent discoveries about PRRs’ dynamic regulation and signaling mechanisms directly leading to downstream molecular events including mitogen-activated protein kinase(MAPK) activation and calcium(Ca2+) burst. Plants also have evolved intracellular NLRs to perceive the presence of specific pathogen effectors and trigger more robust immune responses. We also discuss the current understanding of the mechanisms of NLR activation, which has been greatly advanced by recent breakthroughs including structures of the first full-length plant NLR complex, findings of NLR sensor-helper pairs and novel biochemical activity of Toll/interleukin-1 receptor(TIR) domain.
基金This work was funded by The Max Planck Society, an Alexander von Hum-boldt Foundation postdoctoral fellowship, and the National Nature Science Foundation of China （Grant 31770277） （HC）, a Chinese Scholarship Council PhD fellowship （CSC） （JQ） and Deutsche Forschungsgemein- schaft SFB 670 grant （JEP, DB）.
文摘In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat （NLR） receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 （EDS1） controls transcriptional reprogramming in resistance triggered by Toll-lnterleukinl-Receptor domain （TIR）-family NLRs （TNLs）. Transcriptional induction of the salicylic acid （SA） hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid （JA） hormone pathways. In the TNL immune response, EDSl/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine （COR）. We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.
基金National Natural Science Foundation of China (31471160)the Strategic Priority Research Program of Chinese Academy of Sciences PCDB27030102).
文摘Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The Arabidopsis NLR protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) forms a precomplex with HOPZ-ETI-DEFICIENT 1 (ZED1),a receptor-like cytoplasmic kinase (RLCK) XII-2 subfamily member, to recognize the Pseudomonas syringae effector HopZ1 a. We previously described a dominant mutant of Arabi-dopsis ZED1, zed1-D, which displays temperature-sensitive autoimmunity in a ZAR1-dependent manner. Here, we report that the RLCKs SUPPRESSOR OF ZED1-D1 (SZE1) and SZE2 associate with the ZAR1-ZED1 complex and are required for the ZED7-D-activated autoimmune response and HopZ1a-triggered immunity. We show that SZE1 but not SZE2 has autophosphorylation activity, and that the N-terminal myristoylation of both SZE1 and SZE2 is critical for their plasma membrane localization and ZED1-D-activated autoimmunity. Furthermore, we demonstrate that SZE1 and SZE2 both interact with ZAR1 to form ja functional complex and are required for resistance against P. syringae pv. tomato DC3000 ex-pressing HopZIa. We also provide evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1, leading to its activation. Taken together, our re-sults reveal SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity.
基金supported by grants from the National Natural Science Foundation of China (31761133017)the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB11020100) to D.T
文摘Life or death?It’s a question animal and plant cells ask themselves during development and throughout their lives–and when they choose the latter option,cells can execute a genetically programmed set of cellular functions that result in cell death.In animals and plants,the execution of programmed cell death is critical for proper development and for immunity against invading microbes.
基金supported by National Key Research and Development Program of China (2022YFF1001500)Guiding Project of Fujian Science and Technology Plan(2022N0005)
文摘Plants need to fine-tune defense responses to maintain a robust but flexible host barrier to various pathogens.Helix-loop-helix/basic helix-loop-helix(HLH/bHLH)complexes play important roles in fine-tuning plant development.However,the function of these genes in plant immunity and how they are regulated remain obscure.Here,we identified an atypical bHLH transcription factor,Oryza sativa(Os)HLH46,that interacts with rice receptor-like cytoplasmic kinase(RLCK)Os BRASSINOSTEROID-SIGNALING KINASE1-2(OsBSK1-2),which plays a key role in rice blast resistance.OsBSK1-2 stabilized OsHLH46 both in vivo and in vitro.In addition,OsHLH46 positively regulates rice blast resistance,which depends on OsBSK1-2.OsHLH46 has no transcriptional activation activity and interacts with a typical bHLH protein,OsbHLH6,which negatively regulates rice blast resistance.OsbHLH6 binds to the promoter of OsWRKY45 and inhibits its expression,while OsHLH46 suppresses the function of OsbHLH6 by blocking its DNA binding and transcriptional inhibition of OsWRKY45.Consistent with these findings,OsWRKY45 was up-regulated in OsHLH46-overexpressing plants.In addition,the oshlh46 mutant overexpressing OsbHLH6 is more susceptible to Magnaporthe oryzae than is the wild type,suggesting that OsHLH46 suppresses OsbHLH6-mediated rice blast resistance.Our results not only demonstrated that OsBSK1-2 regulates rice blast resistance via the OsHLH46/OsbHLH6 complex,but also uncovered a new mechanism for plants to fine-tune plant immunity by regulating the HLH/bHLH complex via RLCKs.
基金supported by the Science and Technology Research Program of Chongqing Municipal Education Commission(Grant No.KJQN202201225 to L.R.)the Open Fund of Fujian Provincial Key Laboratory of Eco-Industrial Green Technology(Grant No.WYKF-EIGT2022-6 to L.R.)the National Natural Science Foundation of China(Grant No.32370302 to W.W.).
文摘Mitogen-activated protein kinase(MAPK)activation is one of the significant immune events that respond to pathogens in plants.A MAPK cascade often contains a MAPK kinase kinase(MAPKKK),a MAPK kinase(MAPKK/MKK),and a MAPK.The well-characterized MAPK cascade,to date,is the MAPKKK3/4/5-MKK4/5-MPK3/6 module.Soybean cyst nematodes(SCN)is one of the most devastating soybean pathogens.However,the early immune components contributing to soybean resistance to SCN and the role of the MAPK cascade in the soybean-SCN interaction remain unclear.A recent study published in Plant Cell discovered that GmMPK3/6 phosphorylates a receptor-like cytoplasmic kinase(RLCK),CDG1-LIKE1(GmCDL1),and maintains the stability of GmCDL1 in soybean.Remarkably,GmCDL1 enhances GmMPK3/6 activation and resistance to SCN by phosphorylating GmMAPKKK5 and activating the GmMAPKKK5-GmMKK4-GmMPK3/6 cascade.In addition,two L-type lectin receptor kinases(LecRKs),GmLecRK02g and GmLecRK08g,are involved in the GmCDL1 function after the perception of SCN.taken together,this study not only discovers a complete early immune pathway that responds to SCN infection in soybean,but also reveals a molecular mechanism by which plants maintain the activation of the MAPK cascade and resistance.
基金supported by grants from the National Research Foundation of Korea(NRF)(2018R1A5A1023599,2020R1A2B5B03096402,and 2021M3H9A1096935 to Y.-H.L.and 2019R1I1A1A01059802 to C.-Y.K.).C.-Y.K.is grateful for a graduate fellowship from the Brain Korea 21 Plus Program.
文摘Plants possess effective immune systems that defend against most microbial attackers.Recent plant immunity research has focused on the classic binary defense model involving the pivotal role of small-molecule hormones in regulating the plant defense signaling network.Although most of our current understanding comes from studies that relied on information derived from a limited number of pathosystems,newer studies concerning the incredibly diverse interactions between plants and microbes are providing additional insights into other novel mechanisms.Here,we review the roles of both classical and more recently identified components of defense signaling pathways and stress hormones in regulating the ambivalence effect during responses to diverse pathogens.Because of their different lifestyles,effective defense against biotrophic pathogens normally leads to increased susceptibility to necrotrophs,and vice versa.Given these opposing forces,the plant potentially faces a trade-off when it mounts resistance to a specific pathogen,a phenomenon referred to here as the ambivalence effect.We also highlight a novel mechanism by which translational control of the proteins involved in the ambivalence effect can be used to engineer durable and broad-spectrum disease resistance,regardless of the lifestyle of the invading pathogen.
基金supported by the National Science Fund for Excellent Young Scholars(32022012).
文摘Triticeae species,including wheat,barley,and rye,are critical for global food security.Mapping agronomically important genes is crucial for elucidating molecular mechanisms and improving crops.However,Triticeae includes many wild relatives with desirable agronomic traits,and frequent introgressions occurred during Triticeae evolution and domestication.Thus,Triticeae genomes are generally large and complex,making the localization of genes or functional elements that control agronomic traits challenging.Here,we developed Triti-Map,which contains a suite of user-friendly computational packages specifically designed and optimized to overcome the obstacles of gene mapping in Triticeae,as well as a web interface integrating multi-omics data from Triticeae for the efficient mining of genes or functional elements that control particular traits.The Triti-Map pipeline accepts bothDNA and RNAbulk-segregated sequencing data as well as traditional QTL data as inputs for locating genes and elucidating their functions.We illustrate the usage of Triti-Map with a combination of bulk-segregated ChIP-seq data to detect a wheat disease-resistance gene with its promoter sequence that is absent from the reference genome and clarify its evolutionary process.We hope that Triti-Map will facilitate gene isolation and accelerate Triticeae breeding.
