Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in re...Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in response to biotrophic bacterial infection,remain elusive.Here,we demonstrate that DELLA proteins and EDS1,an essential resistance regulator,form a central module modulating plant growth-defense tradeoffs via direct interaction.When infected by Pst DC3000,EDS1 rapidly promotes salicylic acid(SA)biosynthesis and resistance-related gene expression to prime defense response,while pathogen infection stabilizes DELLA proteins RGA and RGL3 to restrict growth in a partially EDS1-dependent manner,which facilitates plants to develop resistance to pathogens.However,the increasingly accumulated DELLAs interact with EDS1 to suppress SA overproduction and excessive resistance response.Taken together,our findings reveal a DELLA-EDS1-mediated feedback regulatory loop by which plants maintain the subtle balance between growth and defense to avoid excessive growth or defense in response to constant biotrophic pathogen attack.展开更多
Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates p...Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates plant growth and defense in both compatible and incompatible infections.This module consisted of BZR1,a key transcription factor in brassinosteroid(BR)signaling,and EDS1,an essential positive regulator of plant innate immunity.We found that EDS1 interacts with BZR1 and suppresses its transcriptional activ-ities.Consistently,upregulation of EDS1 function by a virulent Pseudomonas syringae strain or salicylic acid treatment inhibited BZR1-regulated expression of BR-responsive genes and BR-promoted growth.Furthermore,we showed that the cytoplasmic fraction of BZR1 positively regulates effector-triggered im-munity(ETI)controlled by the TIR-NB-LRR protein RPS4,which is attenuated by BZR1's nuclear transloca-tion.Mechanistically,cytoplasmic BZR1 facilitated AvrRps4-triggered dissociation of EDS1 and RPS4 by binding to EDS1,thus leading to efficient activation of RPS4-controlled ETI.Notably,transgenic expression of a mutant BZR1 that accumulates exclusively in the cytoplasm improved pathogen resistance without compromising plant growth.Collectively,these results shed new light on plant growth-defense coordina-tion and reveal a previously unknown function for the cytoplasmic fraction of BZR1.The BZR1-EDS1 mod-ule may be harnessed for the simultaneous improvement of crop productivity and pathogen resistance.展开更多
Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this stu...Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this study,we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus,and is required for EDS1 protein accumulation?NPR3 and NPR4,which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase,interact with and mediate the degradation of EDS1 via the 26S proteasome.We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4.Furthermore,we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity.Collectively,our study reveals a novel mechanism by which plants fine-tune defense resporises by inhibiting the degradation of a positive player in plant immunity.展开更多
Plant intracellular nucleotide-binding leucine-rich repeat(NLR)receptors with an N-terminal Toll/Interleukin-1 recep-tor(TIR)domain detect pathogen effectors to produce TIR-catalyzed signaling molecules for activation...Plant intracellular nucleotide-binding leucine-rich repeat(NLR)receptors with an N-terminal Toll/Interleukin-1 recep-tor(TIR)domain detect pathogen effectors to produce TIR-catalyzed signaling molecules for activation of plant immunity.Plant immune signaling by TIR-containing NLR(TNL)proteins converges on Enhanced Disease Suscepti-bility 1(EDS1)and its direct partners Phytoalexin Deficient 4(PAD4)or Senescence-Associated Gene 101(SAG101).TNL signaling also require helper NLRs N requirement gene 1(NRG1)and activated disease resistance 1(ADR1).In two recent remarkable papers published in Science,the authors show that the TIR-containing proteins catalyze and produce two types of signaling molecules,ADPr-ATP/diADPR and pRib-AMP/ADP.Importantly,they demonstrate that EDS1-SAG101 and EDS1-PAD4 modules are the receptor complexes for ADPr-ATP/diADPRp and Rib-AMP/ADP,respec-tively,which allosterically promote EDS1-SAG101 interaction with NRG1 and EDS1-PAD4 interaction with ADR1.Thus,two different small molecules catalyzed by TIR-containing proteins selectively activate the downstream two distinct branches of EDS1-mediated immune signalings.These breakthrough studies significantly advance our understanding of TNL downstream signaling pathway.展开更多
基金This research was supported by grants from the "Strategic PriorityResearch Program " of the Chinese Academy of Sciences (no.XDA13020500)the National Natural Science Foundation of China (no.31300239)and the Natural Science Foundation of Guangdong Province(S2013040013147).
文摘Plants maintain a dynamic balance between growth and defense,and optimize allocation of resources for survival under constant pathogen infections.However,the underlying molecular regulatory mechanisms,especially in response to biotrophic bacterial infection,remain elusive.Here,we demonstrate that DELLA proteins and EDS1,an essential resistance regulator,form a central module modulating plant growth-defense tradeoffs via direct interaction.When infected by Pst DC3000,EDS1 rapidly promotes salicylic acid(SA)biosynthesis and resistance-related gene expression to prime defense response,while pathogen infection stabilizes DELLA proteins RGA and RGL3 to restrict growth in a partially EDS1-dependent manner,which facilitates plants to develop resistance to pathogens.However,the increasingly accumulated DELLAs interact with EDS1 to suppress SA overproduction and excessive resistance response.Taken together,our findings reveal a DELLA-EDS1-mediated feedback regulatory loop by which plants maintain the subtle balance between growth and defense to avoid excessive growth or defense in response to constant biotrophic pathogen attack.
基金supported by grants from the National Natural Science Foundation of China(91935304)the Innovative Postdoctoral Research Initiative of Henan Province(to G.Q.)the National Science Foundation(EAGER grant 1464527 and grant IOS-1758994 to Z.Q.F.).
文摘Plants have developed sophisticated strategies to coordinate growth and immunity,but our understanding of the underlying mechanism remains limited.In this study,we identified a novel molecular module that reg-ulates plant growth and defense in both compatible and incompatible infections.This module consisted of BZR1,a key transcription factor in brassinosteroid(BR)signaling,and EDS1,an essential positive regulator of plant innate immunity.We found that EDS1 interacts with BZR1 and suppresses its transcriptional activ-ities.Consistently,upregulation of EDS1 function by a virulent Pseudomonas syringae strain or salicylic acid treatment inhibited BZR1-regulated expression of BR-responsive genes and BR-promoted growth.Furthermore,we showed that the cytoplasmic fraction of BZR1 positively regulates effector-triggered im-munity(ETI)controlled by the TIR-NB-LRR protein RPS4,which is attenuated by BZR1's nuclear transloca-tion.Mechanistically,cytoplasmic BZR1 facilitated AvrRps4-triggered dissociation of EDS1 and RPS4 by binding to EDS1,thus leading to efficient activation of RPS4-controlled ETI.Notably,transgenic expression of a mutant BZR1 that accumulates exclusively in the cytoplasm improved pathogen resistance without compromising plant growth.Collectively,these results shed new light on plant growth-defense coordina-tion and reveal a previously unknown function for the cytoplasmic fraction of BZR1.The BZR1-EDS1 mod-ule may be harnessed for the simultaneous improvement of crop productivity and pathogen resistance.
基金the National Natural Science Foundation of China(31701863)the University of South Carolina Office of Research(ASPIRE-I TrackllB,13010E244)the Postdoctoral Workstation of Jiangsu Academy of Agricultural Sciences.
文摘Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4.However,the relationships among these important immune regulators remain elusive.In this study,we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus,and is required for EDS1 protein accumulation?NPR3 and NPR4,which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase,interact with and mediate the degradation of EDS1 via the 26S proteasome.We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4.Furthermore,we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity.Collectively,our study reveals a novel mechanism by which plants fine-tune defense resporises by inhibiting the degradation of a positive player in plant immunity.
基金support from the National Natural Science Foundation of China(31925032 and 31870143).
文摘Plant intracellular nucleotide-binding leucine-rich repeat(NLR)receptors with an N-terminal Toll/Interleukin-1 recep-tor(TIR)domain detect pathogen effectors to produce TIR-catalyzed signaling molecules for activation of plant immunity.Plant immune signaling by TIR-containing NLR(TNL)proteins converges on Enhanced Disease Suscepti-bility 1(EDS1)and its direct partners Phytoalexin Deficient 4(PAD4)or Senescence-Associated Gene 101(SAG101).TNL signaling also require helper NLRs N requirement gene 1(NRG1)and activated disease resistance 1(ADR1).In two recent remarkable papers published in Science,the authors show that the TIR-containing proteins catalyze and produce two types of signaling molecules,ADPr-ATP/diADPR and pRib-AMP/ADP.Importantly,they demonstrate that EDS1-SAG101 and EDS1-PAD4 modules are the receptor complexes for ADPr-ATP/diADPRp and Rib-AMP/ADP,respec-tively,which allosterically promote EDS1-SAG101 interaction with NRG1 and EDS1-PAD4 interaction with ADR1.Thus,two different small molecules catalyzed by TIR-containing proteins selectively activate the downstream two distinct branches of EDS1-mediated immune signalings.These breakthrough studies significantly advance our understanding of TNL downstream signaling pathway.
