EDR2 is a negative regulator of the defense response and cell death in Arabidopsis.Loss-of-function of EDR2 leads to enhanced resistance to powdery mildew.To identify new components in the EDR2 signal transduction pat...EDR2 is a negative regulator of the defense response and cell death in Arabidopsis.Loss-of-function of EDR2 leads to enhanced resistance to powdery mildew.To identify new components in the EDR2 signal transduction pathway,mutations that suppress edr2 resistant phenotypes were screened.Three mutants,edts5-1,edts5-2 and edts5-3（edr two suppressor 5）,were identified.The EDTS5 gene was identified by map-based cloning and previously was shown to encode an aminotransferase（ALD1）.Therefore we renamed these three alleles ald1-10,ald1-11 and ald1-12,respectively.Mutations in ALD1 suppressed all edr2-mediated phenotypes,including powdery mildew resistance,programmed cell death and ethylene-induced senescence.Accumulation of hydrogen peroxide in edr2 was also suppressed by ald1 mutation.The expression of defense-related genes was up-regulated in the edr2 mutant,and the up-regulation of those genes in edr2 was suppressed in the edr2/ald1 double mutant.The ald1 single mutant displayed delayed ethylene-induced senescence.In addition,ald1 mutation suppressed edr1-mediated powdery mildew resistance,but could not suppress the edr11edr2 double-mutant phenotype.These data demonstrate that ALD1 plays important roles in edr2-mediated defense responses and senescence,and revealed a crosstalk between ethylene and salicylic acid signaling mediated by ALD1 and EDR2.展开更多
Chloroplasts are central to plant immunity,with the chloroplast-localized protein AGD2-LIKE DEFENSE RESPONSE PROTEIN 1(ALD1)playing a critical role in producing pipecolic acid(Pip),a key immune signal.However,the regu...Chloroplasts are central to plant immunity,with the chloroplast-localized protein AGD2-LIKE DEFENSE RESPONSE PROTEIN 1(ALD1)playing a critical role in producing pipecolic acid(Pip),a key immune signal.However,the regulation of ALD1 and how pathogens evade ALD1-mediated defenses remain poorly understood.Using the geminivirus tomato yellow leaf curl China virus and its associated betasatellite(TYLCCNV/TYLCCNB)as a model,we uncovered a defense mechanism involving organellar single-stranded DNA-binding protein 1(OSB1),which stabilizes ALD1 and promotes Pip biosynthesis to strengthen immunity.Crucially,the viralβC1 effector encoded by TYLCCNB disrupts this pathway by binding OSB1 and sequestering it away from chloroplasts,thereby blocking OSB1-ALD1 interaction,destabilizing ALD1,and suppressing Pip-dependent defenses.Strikingly,βC1 mutants defective in OSB1 binding fail to interfere with the OSB1-ALD1 stability,and TYLCCNV infections carrying these mutants induce attenuated symptoms in Nicotiana benthamiana.Our study not only reveals how ALD1-OSB1 cooperates in chloroplast immunity but also demonstrates how geminiviruses,as a tractable model,can dissect pathogen counter-defense strategies.展开更多
Cytokines are considered crucial players in inflammatory-associated disorders throughout the body.Fatty liver diseases such as alcoholic liver disease(ALD)and non-alcoholic fatty liver disease(NAFLD)are commonly chara...Cytokines are considered crucial players in inflammatory-associated disorders throughout the body.Fatty liver diseases such as alcoholic liver disease(ALD)and non-alcoholic fatty liver disease(NAFLD)are commonly characterized by lipid accumulation and in a substantial subset of patients with inflammation in the liver.Amount of inflammation affects long-term outcome of liver disease including evolution of liver fibrosis,cirrhosis and hepatocellular carcinoma.Especially the pro-inflammatory cytokines Interleukin(IL)-1(αandβ)and tumor necrosis factor(TNF)αplay a central role in many stages of liver diseases mediating fundamental aspects of those diseases including acute phase protein synthesis,lipid metabolism,cholestasis and degree of fibrosis.These key cytokines released mainly by mononuclear cells affect all liver cell types and orchestrate the production of many other mediators relevant in chronic liver diseases.Inflammatory cytokines also regulate crucially the development of insulin resistance,a key component of NAFLD.Blocking these critical mediators of inflammation by specific antibodies,especially TNFα,has so far not been proven successful in alcoholic steatohepatitis,a cytokine-driven disorder.In summary,inflammatory cytokines are continuously present locally and systemically in patients with advanced fatty liver diseases,mediating and affecting the clinical phenotype and many features of these disorders.展开更多
基金supported by the grants from National Basic Research Program of China (973 Program, 2011CB100700)the National Transgenic Program of China (No. 2009ZX08009-042B)the National Natural Science Foundation of China (No. 30771168).
文摘EDR2 is a negative regulator of the defense response and cell death in Arabidopsis.Loss-of-function of EDR2 leads to enhanced resistance to powdery mildew.To identify new components in the EDR2 signal transduction pathway,mutations that suppress edr2 resistant phenotypes were screened.Three mutants,edts5-1,edts5-2 and edts5-3（edr two suppressor 5）,were identified.The EDTS5 gene was identified by map-based cloning and previously was shown to encode an aminotransferase（ALD1）.Therefore we renamed these three alleles ald1-10,ald1-11 and ald1-12,respectively.Mutations in ALD1 suppressed all edr2-mediated phenotypes,including powdery mildew resistance,programmed cell death and ethylene-induced senescence.Accumulation of hydrogen peroxide in edr2 was also suppressed by ald1 mutation.The expression of defense-related genes was up-regulated in the edr2 mutant,and the up-regulation of those genes in edr2 was suppressed in the edr2/ald1 double mutant.The ald1 single mutant displayed delayed ethylene-induced senescence.In addition,ald1 mutation suppressed edr1-mediated powdery mildew resistance,but could not suppress the edr11edr2 double-mutant phenotype.These data demonstrate that ALD1 plays important roles in edr2-mediated defense responses and senescence,and revealed a crosstalk between ethylene and salicylic acid signaling mediated by ALD1 and EDR2.
基金supported by the National Key Research and Development Program of China(2021YFD1400400)to Fangfang Lithe National Natural Science Foundation of China(W2411024)to Xueping Zhou,respectively.
文摘Chloroplasts are central to plant immunity,with the chloroplast-localized protein AGD2-LIKE DEFENSE RESPONSE PROTEIN 1(ALD1)playing a critical role in producing pipecolic acid(Pip),a key immune signal.However,the regulation of ALD1 and how pathogens evade ALD1-mediated defenses remain poorly understood.Using the geminivirus tomato yellow leaf curl China virus and its associated betasatellite(TYLCCNV/TYLCCNB)as a model,we uncovered a defense mechanism involving organellar single-stranded DNA-binding protein 1(OSB1),which stabilizes ALD1 and promotes Pip biosynthesis to strengthen immunity.Crucially,the viralβC1 effector encoded by TYLCCNB disrupts this pathway by binding OSB1 and sequestering it away from chloroplasts,thereby blocking OSB1-ALD1 interaction,destabilizing ALD1,and suppressing Pip-dependent defenses.Strikingly,βC1 mutants defective in OSB1 binding fail to interfere with the OSB1-ALD1 stability,and TYLCCNV infections carrying these mutants induce attenuated symptoms in Nicotiana benthamiana.Our study not only reveals how ALD1-OSB1 cooperates in chloroplast immunity but also demonstrates how geminiviruses,as a tractable model,can dissect pathogen counter-defense strategies.
基金H.Tilg was supported by the excellence initiative(Competence Centers for Excellent Technologies-COMET)of the Austrian Research Promotion Agency(Forschungsforderungsgesellschaft,FFG):Research Center of Excellence in Vascular Ageing Tyrol,VASCage(K-Project Nr.843536)funded by the Federal Ministry for Transport,Innovation and Technology(BMVIT),Bundesministerium für Wissenschaft Forschung und Wirtschaft(BMWFW),the Wirtschaftsagentur Wien and the Standortagentur Tirol.
文摘Cytokines are considered crucial players in inflammatory-associated disorders throughout the body.Fatty liver diseases such as alcoholic liver disease(ALD)and non-alcoholic fatty liver disease(NAFLD)are commonly characterized by lipid accumulation and in a substantial subset of patients with inflammation in the liver.Amount of inflammation affects long-term outcome of liver disease including evolution of liver fibrosis,cirrhosis and hepatocellular carcinoma.Especially the pro-inflammatory cytokines Interleukin(IL)-1(αandβ)and tumor necrosis factor(TNF)αplay a central role in many stages of liver diseases mediating fundamental aspects of those diseases including acute phase protein synthesis,lipid metabolism,cholestasis and degree of fibrosis.These key cytokines released mainly by mononuclear cells affect all liver cell types and orchestrate the production of many other mediators relevant in chronic liver diseases.Inflammatory cytokines also regulate crucially the development of insulin resistance,a key component of NAFLD.Blocking these critical mediators of inflammation by specific antibodies,especially TNFα,has so far not been proven successful in alcoholic steatohepatitis,a cytokine-driven disorder.In summary,inflammatory cytokines are continuously present locally and systemically in patients with advanced fatty liver diseases,mediating and affecting the clinical phenotype and many features of these disorders.
