Nucleotide binding,leucine-rich repeat(NB-LRR)proteins are critical for disease resistance in plants,while we do not know whether S-acylation of these proteins plays a role during bacterial infection.We identified 30 ...Nucleotide binding,leucine-rich repeat(NB-LRR)proteins are critical for disease resistance in plants,while we do not know whether S-acylation of these proteins plays a role during bacterial infection.We identified 30 Arabidopsis mutants with mutations in NB-LRR encoding genes from the Nottingham Arabidopsis Stock Center and characterized their contribution to the plant immune response after inoculation with Pseudomonas syringae pv tomato DC3000(Pst DC3000).Of the five mutants that were hyper-susceptible to the pathogen,three(R5L1,R5L2 and RPS5)proteins contain the conserved S-acylation site in the N-terminal coiled-coil(CC)domain.In wild-type(WT)Arabidopsis plants,R5L1 was transcriptionally activated upon pathogen infection,and R5L1 overexpression lines had enhanced resistance.Independent experiments indicated that R5L1 localized at the plasma membrane(PM)via S-acylation of its N-terminal CC domain,which was mediated by PROTEIN S-ACYL TRANSFERASE 13/16(PAT13,PAT16).Modification of the S-acylation site reduced its affinity for binding the PM,with a consequent significant reduction in bacterial resistance.PM localization of R5L1 was significantly reduced in pat13 and pat16 mutants,similar to what was found for WT plants treated with 2-bromopalmitate,an S-acylationblocking agent.Transgenic plants expressing R5L1 in the pat13 pat16 double mutant showed no enhanced disease resistance.Overexpression of R5L1 in WT Arabidopsis resulted in substantial accumulation of reactive oxygen species after inoculation with Pst DC3000;this effect was not observed with a mutant R5L1 carrying a mutated Sacylation site.Our data suggest that PAT13-and PAT16-mediated S-acylation of R5L1 is crucial for its membrane localization to activate the plant defense response.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
基金supported by grants from the National Natural Science Foundation of China(31830057 and 31690091 to Y.-X.Z.)the National Postdoctoral Program for Innovative Talent(BX20200008 to G.H.)。
文摘Nucleotide binding,leucine-rich repeat(NB-LRR)proteins are critical for disease resistance in plants,while we do not know whether S-acylation of these proteins plays a role during bacterial infection.We identified 30 Arabidopsis mutants with mutations in NB-LRR encoding genes from the Nottingham Arabidopsis Stock Center and characterized their contribution to the plant immune response after inoculation with Pseudomonas syringae pv tomato DC3000(Pst DC3000).Of the five mutants that were hyper-susceptible to the pathogen,three(R5L1,R5L2 and RPS5)proteins contain the conserved S-acylation site in the N-terminal coiled-coil(CC)domain.In wild-type(WT)Arabidopsis plants,R5L1 was transcriptionally activated upon pathogen infection,and R5L1 overexpression lines had enhanced resistance.Independent experiments indicated that R5L1 localized at the plasma membrane(PM)via S-acylation of its N-terminal CC domain,which was mediated by PROTEIN S-ACYL TRANSFERASE 13/16(PAT13,PAT16).Modification of the S-acylation site reduced its affinity for binding the PM,with a consequent significant reduction in bacterial resistance.PM localization of R5L1 was significantly reduced in pat13 and pat16 mutants,similar to what was found for WT plants treated with 2-bromopalmitate,an S-acylationblocking agent.Transgenic plants expressing R5L1 in the pat13 pat16 double mutant showed no enhanced disease resistance.Overexpression of R5L1 in WT Arabidopsis resulted in substantial accumulation of reactive oxygen species after inoculation with Pst DC3000;this effect was not observed with a mutant R5L1 carrying a mutated Sacylation site.Our data suggest that PAT13-and PAT16-mediated S-acylation of R5L1 is crucial for its membrane localization to activate the plant defense response.
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.
