scholarly journals A 2′-O-Methyltransferase Responsible for Transfer RNA Anticodon Modification Is Pivotal for Resistance to Pseudomonas syringae DC3000 in Arabidopsis

2018 ◽  
Vol 31 (12) ◽  
pp. 1323-1336 ◽  
Author(s):  
Vicente Ramírez ◽  
Beatriz González ◽  
Ana López ◽  
Maria Jose Castelló ◽  
Maria José Gil ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Bacterial Pathogen ◽  
Transfer Rna ◽  
Resistance Response ◽  
Chemical Structures ◽  
Trna Modifications ◽  
Trna Species ◽  
Living Organisms ◽  
And Function

Transfer RNA (tRNA) is the most highly modified class of RNA species in all living organisms. Recent discoveries have revealed unprecedented complexity in the tRNA chemical structures, modification patterns, regulation, and function, suggesting that each modified nucleoside in tRNA may have its own specific function. However, in plants, our knowledge of the role of individual tRNA modifications and how they are regulated is very limited. In a genetic screen designed to identify factors regulating disease resistance in Arabidopsis, we identified SUPPRESSOR OF CSB3 9 (SCS9). Our results reveal SCS9 encodes a tRNA methyltransferase that mediates the 2′-O-ribose methylation of selected tRNA species in the anticodon loop. These SCS9-mediated tRNA modifications enhance susceptibility during infection with the virulent bacterial pathogen Pseudomonas syringae DC3000. Lack of such tRNA modification, as observed in scs9 mutants, specifically dampens plant resistance against DC3000 without compromising the activation of the salicylic acid signaling pathway or the resistance to other biotrophic pathogens. Our results support a model that gives importance to the control of certain tRNA modifications for mounting an effective disease resistance in Arabidopsis toward DC3000 and, therefore, expands the repertoire of molecular components essential for an efficient disease resistance response.

scholarly journals Pseudomonas syringae Effector AvrPphB Suppresses AvrB-Induced Activation of RPM1 but Not AvrRpm1-Induced Activation

2015 ◽  
Vol 28 (6) ◽  
pp. 727-735 ◽  
Author(s):  
Andrew R. Russell ◽  
Tom Ashfield ◽  
Roger W. Innes
Keyword(s):  
Disease Resistance ◽  
Protein Kinase ◽  
Molecular Mechanism ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Hypersensitive Resistance ◽  
Nicotiana Glutinosa ◽  
Resistance Response ◽  
Interacting Protein ◽  
Soybean Plants

The Pseudomonas syringae effector AvrB triggers a hypersensitive resistance response in Arabidopsis and soybean plants expressing the disease resistance (R) proteins RPM1 and Rpg1b, respectively. In Arabidopsis, AvrB induces RPM1-interacting protein kinase (RIPK) to phosphorylate a disease regulator known as RIN4, which subsequently activates RPM1-mediated defenses. Here, we show that AvrPphB can suppress activation of RPM1 by AvrB and this suppression is correlated with the cleavage of RIPK by AvrPphB. Significantly, AvrPphB does not suppress activation of RPM1 by AvrRpm1, suggesting that RIPK is not required for AvrRpm1-induced modification of RIN4. This observation indicates that AvrB and AvrRpm1 recognition is mediated by different mechanisms in Arabidopsis, despite their recognition being determined by a single R protein. Moreover, AvrB recognition but not AvrRpm1 recognition is suppressed by AvrPphB in soybean, suggesting that AvrB recognition requires a similar molecular mechanism in soybean and Arabidopsis. In support of this, we found that phosphodeficient mutations in the soybean GmRIN4a and GmRIN4b proteins are sufficient to block Rpg1b-mediated hypersensitive response in transient assays in Nicotiana glutinosa. Taken together, our results indicate that AvrB and AvrPphB target a conserved defense signaling pathway in Arabidopsis and soybean that includes RIPK and RIN4.

scholarly journals Isolation of New Arabidopsis Mutants With Enhanced Disease Susceptibility to Pseudomonas syringae by Direct Screening

Genetics ◽  
1998 ◽  
Vol 149 (2) ◽  
pp. 537-548
Author(s):  
Sigrid M Volko ◽  
Thomas Boller ◽  
Frederick M Ausubel
Keyword(s):  
Pseudomonas Syringae ◽  
Fungal Pathogen ◽  
Systemic Acquired Resistance ◽  
Disease Susceptibility ◽  
Acquired Resistance ◽  
Bacterial Pathogen ◽  
Avirulent Strain ◽  
Resistance Response ◽  
Arabidopsis Mutants ◽  
Pathogen Response

Abstract To identify plant defense components that are important in restricting the growth of virulent pathogens, we screened for Arabidopsis mutants in the accession Columbia (carrying the transgene BGL2-GUS) that display enhanced disease susceptibility to the virulent bacterial pathogen Pseudomonas syringae pv. maculicola (Psm) ES4326. Among six (out of a total of 11 isolated) enhanced disease susceptibility (eds) mutants that were studied in detail, we identified one allele of the previously described npr1/nim1/sai1 mutation, which is affected in mounting a systemic acquired resistance response, one allele of the previously identified EDS5 gene, and four EDS genes that have not been previously described. The six eds mutants studied in detail (npr1-4, eds5-2, eds10-1, eds11-1, eds12-1, and eds13-1) displayed different patterns of enhanced susceptibility to a variety of phytopathogenic bacteria and to the obligate biotrophic fungal pathogen Erysiphe orontii, suggesting that particular EDS genes have pathogen-specific roles in conferring resistance. All six eds mutants retained the ability to mount a hypersensitive response and to restrict the growth of the avirulent strain Psm ES4326/avrRpt2. With the exception of npr1-4, the mutants were able to initiate a systemic acquired resistance (SAR) response, although enhanced growth of Psm ES4326 was still detectable in leaves of SAR-induced plants. The data presented here indicate that eds genes define a variety of components involved in limiting pathogen growth, that many additional EDS genes remain to be discovered, and that direct screens for mutants with altered susceptibility to pathogens are helpful in the dissection of complex pathogen response pathways in plants.

scholarly journals Heterologous Expression of the Constitutive Disease Resistance 2 and 8 Genes from Poncirus trifoliata Restored the Hypersensitive Response and Resistance of Arabidopsis cdr1 Mutant to Bacterial Pathogen Pseudomonas syringae

Plants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 821
Author(s):  
Xiaobao Ying ◽  
Bryce Redfern ◽  
Frederick G. Gmitter ◽  
Zhanao Deng
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Plant Disease Resistance ◽  
Marker Gene ◽  
Bacterial Pathogen ◽  
The United States ◽  
Poncirus Trifoliata ◽  
Close Relative ◽  
Arabidopsis Mutants

Huanglongbing (HLB), also known as citrus greening, is the most destructive disease of citrus worldwide. In the United States, this disease is associated with a phloem-restricted bacterium, Candidatus Liberibacter asiaticus. Commercial citrus cultivars are susceptible to HLB, but Poncirus trifoliata, a close relative of Citrus, is highly tolerant of HLB. Isolating P. trifoliata gene(s) controlling its HLB tolerance followed by expressing the gene(s) in citrus is considered a potential cisgenic approach to engineering citrus for tolerance to HLB. Previous gene expression studies indicated that the constitutive disease resistance (CDR) genes in P. trifoliata (PtCDRs) may play a vital role in its HLB tolerance. This study was designed to use Arabidopsis mutants as a model system to confirm the function of PtCDRs in plant disease resistance. PtCDR2 and PtCDR8 were amplified from P. trifoliata cDNA and transferred into the Arabidopsis cdr1 mutant, whose resident CDR1 gene was disrupted by T-DNA insertion. The PtCDR2 and PtCDR8 transgenic Arabidopsis cdr1 mutant restored its hypersensitive response to the bacterial pathogen Pseudomonas syringae pv. tomato strain DC3000 (Pst DC3000) expressing avrRpt2. The defense marker gene PATHOGENESIS RELATED 1 (PR1) expressed at much higher levels in the PtCDR2 or PtCDR8 transgenic cdr1 mutant than in the non-transgenic cdr1 mutant with or without pathogen infection. Multiplication of Pst DC3000 bacteria in Arabidopsis was inhibited by the expression of PtCDR2 and PtCDR8. Our results showed that PtCDR2 and PtCDR8 were functional in Arabidopsis and played a positive role in disease resistance and demonstrated that Arabidopsis mutants can be a useful alternate system for screening Poncirus genes before making the time-consuming effort to transfer them into citrus, a perennial woody plant that is highly recalcitrant for Agrobacterium or biolistic-mediated transformation.

scholarly journals Suppressors of the Arabidopsis lsd5 Cell Death Mutation Identify Genes Involved in Regulating Disease Resistance Responses

Genetics ◽  
1999 ◽  
Vol 151 (1) ◽  
pp. 305-319
Author(s):  
Jean-Benoit Morel ◽  
Jeffery L Dangl
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Plant Disease Resistance ◽  
Plant Disease ◽  
Disease Susceptibility ◽  
Bacterial Pathogen ◽  
Hypersensitive Reaction ◽  
Cell Death Phenotype ◽  
New Mutations

Abstract Cell death is associated with the development of the plant disease resistance hypersensitive reaction (HR). Arabidopsis lsd mutants that spontaneously exhibit cell death reminiscent of the HR were identified previously. To study further the regulatory context in which cell death acts during disease resistance, one of these mutants, lsd5, was used to isolate new mutations that suppress its cell death phenotype. Using a simple lethal screen, nine lsd5 cell death suppressors, designated phx (for the mythological bird Phoenix that rises from its ashes), were isolated. These mutants were characterized with respect to their response to a bacterial pathogen and oomycete parasite. The strongest suppressors—phx2, 3, 6, and 11-1—showed complex, differential patterns of disease resistance modifications. These suppressors attenuated disease resistance to avirulent isolates of the biotrophic Peronospora parasitica pathogen, but only phx2 and phx3 altered disease resistance to avirulent strains of Pseudomonas syringae pv tomato. Therefore, some of these phx mutants define common regulators of cell death and disease resistance. In addition, phx2 and phx3 exhibited enhanced disease susceptibility to different virulent pathogens, confirming probable links between the disease resistance and susceptibility pathways.

scholarly journals A gossypol biosynthetic intermediate disturbs plant defence response

2019 ◽  
Vol 374 (1767) ◽  
pp. 20180319 ◽  
Author(s):  
Xiu Tian ◽  
Xin Fang ◽  
Jin-Quan Huang ◽  
Ling-Jian Wang ◽  
Ying-Bo Mao ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Plant Disease Resistance ◽  
Map Kinases ◽  
Plant Defence ◽  
Plant Secondary Metabolites ◽  
Bacterial Pathogen ◽  
Defence Response ◽  
Light Reaction ◽  
Highly Active

Plant secondary metabolites and their biosynthesis have attracted great interest, but investigations of the activities of hidden intermediates remain rare. Gossypol and related sesquiterpenes are the major phytoalexins in cotton. Among the six biosynthetic intermediates recently identified, 8-hydroxy-7-keto-δ-cadinene (C234) crippled the plant disease resistance when accumulated upon gene silencing. C234 harbours an α,β-unsaturated carbonyl thus is a reactive electrophile species. Here, we show that C234 application also dampened the Arabidopsis resistance against the bacterial pathogen Pseudomonas syringae pv. maculicola ( Psm ). We treated Arabidopsis with C234, Psm and ( Psm +C234), and analysed the leaf transcriptomes. While C234 alone exerted a mild effect, it greatly stimulated an over-response to the pathogen. Of the 7335 genes affected in the ( Psm +C234)-treated leaves, 3476 were unresponsive without the chemical, in which such functional categories as ‘nucleotides transport’, ‘vesicle transport’, ‘MAP kinases’, ‘G-proteins’, ‘protein assembly and cofactor ligation’ and ‘light reaction’ were enriched, suggesting that C234 disturbed certain physiological processes and the protein complex assembly, leading to distorted defence response and decreased disease resistance. As C234 is efficiently metabolized by CYP71BE79, plants of cotton lineage have evolved a highly active enzyme to prevent the phytotoxic intermediate accumulation during gossypol pathway evolution. This article is part of the theme issue ‘Biotic signalling sheds light on smart pest management’.

scholarly journals Arabidopsis MAPKKK δ-1 is required for full immunity against bacterial and fungal infection

2019 ◽  
Vol 71 (6) ◽  
pp. 2085-2097 ◽  
Author(s):  
Tomoya Asano ◽  
Thi Hang-Ni Nguyen ◽  
Michiko Yasuda ◽  
Yasir Sidiq ◽  
Kohji Nishimura ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Fungal Infection ◽  
Pseudomonas Syringae ◽  
Fusarium Species ◽  
Bacterial Pathogen ◽  
Mitogen Activated Protein Kinase ◽  
Trichothecene Mycotoxin ◽  
Mitogen Activated Protein

Abstract The genome of Arabidopsis encodes more than 60 mitogen-activated protein kinase kinase (MAPKK) kinases (MAPKKKs); however, the functions of most MAPKKKs and their downstream MAPKKs are largely unknown. Here, MAPKKK δ-1 (MKD1), a novel Raf-like MAPKKK, was isolated from Arabidopsis as a subunit of a complex including the transcription factor AtNFXL1, which is involved in the trichothecene phytotoxin response and in disease resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (PstDC3000). A MKD1-dependent cascade positively regulates disease resistance against PstDC3000 and the trichothecene mycotoxin-producing fungal pathogen Fusarium sporotrichioides. MKD1 expression was induced by trichothecenes derived from Fusarium species. MKD1 directly interacted with MKK1 and MKK5 in vivo, and phosphorylated MKK1 and MKK5 in vitro. Correspondingly, mkk1 mutants and MKK5RNAi transgenic plants showed enhanced susceptibility to F. sporotrichioides. MKD1 was required for full activation of two MAPKs (MPK3 and MPK6) by the T-2 toxin and flg22. Finally, quantitative phosphoproteomics suggested that an MKD1-dependent cascade controlled phosphorylation of a disease resistance protein, SUMO, and a mycotoxin-detoxifying enzyme. Our findings suggest that the MKD1–MKK1/MKK5–MPK3/MPK6-dependent signaling cascade is involved in the full immune responses against both bacterial and fungal infection.

scholarly journals Ascorbic Acid Deficiency in Arabidopsis Induces Constitutive Priming That is Dependent on Hydrogen Peroxide, Salicylic Acid, and the NPR1 Gene

2010 ◽  
Vol 23 (3) ◽  
pp. 340-351 ◽  
Author(s):  
Madhumati Mukherjee ◽  
Katherine E. Larrimore ◽  
Naushin J. Ahmed ◽  
Tyler S. Bedick ◽  
Nadia T. Barghouthi ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Messenger Rna ◽  
Bacterial Pathogen ◽  
Pathogen Resistance ◽  
Wild Type ◽  
Pr Genes ◽  
Pathogenesis Related

The ascorbic acid (AA)-deficient Arabidopsis thaliana vtc1-1 mutant exhibits increased resistance to the virulent bacterial pathogen Pseudomonas syringae. This response correlates with heightened levels of salicylic acid (SA), which induces antimicrobial pathogenesis-related (PR) proteins. To determine if SA-mediated, enhanced disease resistance is a general phenomenon of AA deficiency, to elucidate the signal that stimulates SA synthesis, and to identify the biosynthetic pathway through which SA accumulates, we studied the four AA-deficient vtc1-1, vtc2-1, vtc3-1, and vtc4-1 mutants. We also studied double mutants defective in the AA-biosynthetic gene VTC1 and the SA signaling pathway genes PAD4, EDS5, and NPR1, respectively. All vtc mutants were more resistant to P. syringae than the wild type. With the exception of vtc4-1, this correlated with constitutively upregulated H2O2, SA, and messenger RNA levels of PR genes. Double mutants exhibited decreased SA levels and enhanced susceptibility to P. syringae compared with the wild type, suggesting that vtc1-1 requires functional PAD4, EDS5, and NPR1 for SA biosynthesis and pathogen resistance. We suggest that AA deficiency causes constitutive priming through a buildup of H2O2 that stimulates SA accumulation, conferring enhanced disease resistance in vtc1-1, vtc2-1, and vtc3-1, whereas vtc4-1 might be sensitized to H2O2 and SA production after infection.

scholarly journals Two Chloroplast-Localized Proteins: AtNHR2A and AtNHR2B, Contribute to Callose Deposition During Nonhost Disease Resistance in Arabidopsis

2018 ◽  
Vol 31 (12) ◽  
pp. 1280-1290 ◽  
Author(s):  
Raksha Singh ◽  
Seonghee Lee ◽  
Laura Ortega ◽  
Vemanna S. Ramu ◽  
Muthappa Senthil-Kumar ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Fluorescent Protein ◽  
Bacterial Pathogen ◽  
Virus Induced Gene Silencing ◽  
Wild Type ◽  
Orthologous Genes ◽  
Callose Deposition ◽  
Complex Process ◽  
Physical And Chemical

Plants are naturally resistant to most pathogens through a broad and durable defense response called nonhost disease resistance. Nonhost disease resistance is a complex process that includes preformed physical and chemical barriers and induced responses. In spite of its importance, many components of nonhost disease resistance remain to be identified and characterized. Using virus-induced gene silencing in Nicotiana benthamiana, we discovered a novel gene that we named NbNHR2 (N. benthamiana nonhost resistance 2). NbNHR2-silenced plants were susceptible to the nonadapted pathogen Pseudomonas syringae pv. tomato T1, which does not cause disease in wild-type or nonsilenced N. benthamiana plants. We found two orthologous genes in Arabidopsis thaliana: AtNHR2A and AtNHR2B. Similar to the results obtained in N. benthamiana, Atnhr2a and Atnhr2b mutants were susceptible to the nonadapted bacterial pathogen of A. thaliana, P. syringae pv. tabaci. We further found that these mutants were also defective in callose deposition. AtNHR2A and AtNHR2B fluorescent protein fusions transiently expressed in N. benthamiana localized predominantly to chloroplasts and a few unidentified dynamic puncta. RFP-AtNHR2A and AtNHR2B-GFP displayed overlapping signals in chloroplasts, indicating that the two proteins could interact, an idea supported by coimmunoprecipitation studies. We propose that AtNHR2A and AtNHR2B are new components of a chloroplast-signaling pathway that activates callose deposition to the cell wall in response to bacterial pathogens.

scholarly journals 289 GENOTYPIC DIFFERENCES IN THE INDUCTION OF DISEASE RESISTANCE WITHIN CUCUMIS SATIVUS

HortScience ◽  
1994 ◽  
Vol 29 (5) ◽  
pp. 471d-471
Author(s):  
Lavetta Newell ◽  
Irvin Widders ◽  
Raymond Hammerschmidt
Keyword(s):  
Disease Resistance ◽  
Cucumis Sativus ◽  
Pseudomonas Syringae ◽  
Inbred Lines ◽  
Systemic Resistance ◽  
Genotypic Differences ◽  
Fresh Market ◽  
Resistance Response ◽  
Banding Patterns ◽  
Pickling Cucumbers

Systemic resistance to necrotic lesion forming pathogens can be induced in certain plant species by inoculating a young leaf with a limited amount of pathogen or by treating with specific non-pesticidal chemical compounds. A physiological change correlated with the induced resistance response is an increase in the activity of acidic apoplastic peroxidases. When seedlings of 17 inbred lines of fresh market and pickling cucumbers were foliar treated with 20 ppm 2,6-dichloroisonicotinic acid (Ciba Geigy 41396) and subsequently inoculated with either Pseudomonas syringae pv. lachrymans or Colletotrichum lagenarium, significant differences were observed in the number of lesions that developed. CG 41396 treatment also gave rise to 4-fold (Producer and Early Russian), 3-fold (Poinsett and Straight 8) and 2-fold (Delcrow, WI 2757, TMG-1, TG 72) increases in peroxidase activity within inbred lines. Distinct changes in acid peroxidase electrophoretic isozyme banding patterns were observed within certain inbred lines after treatment with CG 41396. These results indicate that genetic variability exists within Cucumis sativus with respect to plant response to physiological disease resistance inducing treatments.

scholarly journals AtERF11 is a positive regulator for disease resistance against a bacterial pathogen, Pseudomonas syringae, in Arabidopsis thaliana

2007 ◽  
Vol 17 (2) ◽  
pp. 235-240
Author(s):  
Tack-Min Kwon ◽  
Yun-Hui Jung ◽  
Soon-Jae Jeong ◽  
Young-Byung Yi ◽  
Jae-Sung Nam
Keyword(s):  
Arabidopsis Thaliana ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Bacterial Pathogen ◽  
Positive Regulator
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