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 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 Constitutive Expression of hrap Gene in Transgenic Tobacco Plant Enhances Resistance Against Virulent Bacterial Pathogens by Induction of a Hypersensitive Response

2002 ◽  
Vol 15 (8) ◽  
pp. 764-773 ◽  
Author(s):  
Mang-jye Ger ◽  
Cheng-hsien Chen ◽  
Shaw-yhi Hwang ◽  
Hsiang-en Huang ◽  
Appa Rao Podile ◽  
...  
Keyword(s):  
Disease Resistance ◽  
Transgenic Tobacco ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Plant Disease Resistance ◽  
Constitutive Expression ◽  
Sweet Pepper ◽  
Blue Staining ◽  
Wild Type ◽  
Pathogen Infection

Hypersensitive response-assisting protein (HRAP) has been previously reported as an amphipathic plant protein isolated from sweet pepper that intensifies the harpinPss-mediated hypersensitive response (HR). The hrap gene has no appreciable similarity to any other known sequences, and its activity can be rapidly induced by incompatible pathogen infection. To assess the function of the hrap gene in plant disease resistance, the CaMV 35S promoter was used to express sweet pepper hrap in transgenic tobacco. Compared with wild-type tobacco, transgenic tobacco plants exhibit more sensitivity to harpinPss and show resistance to virulent pathogens (Pseudomonas syringae pv. tabaci and Erwinia carotovora subsp. carotovora). This disease resistance of transgenic tobacco does not originate from a constitutive HR, because endogenous level of salicylic acid and hsr203J mRNA showed similarities in transgenic and wild-type tobacco under noninfected conditions. However, following a virulent pathogen infection in hrap transgenic tobacco, hsr203J was rapidly induced and a micro-HR necrosis was visualized by trypan blue staining in the infiltration area. Consequently, we suggest that the disease resistance of transgenic plants may result from the induction of a HR by a virulent pathogen infection.

scholarly journals The involvement of two epoxide hydrolase genes, NbEH1.1 and NbEH1.2, of Nicotiana benthamiana in the interaction with Colletotrichum destructivum, Colletotrichum orbiculare or Pseudomonas syringae pv. tabaci

2008 ◽  
Vol 35 (11) ◽  
pp. 1112 ◽  
Author(s):  
C. P. Wijekoon ◽  
P. H. Goodwin ◽  
T. Hsiang
Keyword(s):  
Pseudomonas Syringae ◽  
Nicotiana Benthamiana ◽  
Epoxide Hydrolase ◽  
Virus Induced Gene Silencing ◽  
Colletotrichum Orbiculare ◽  
Hypersensitive Resistance ◽  
Resistance Response ◽  
Colletotrichum Destructivum ◽  
Vicinal Diols ◽  
Epoxy Alcohols

Epoxide hydrolase hydrates epoxides to vicinal diols in the phyto-oxylipin peroxygenase pathway resulting in the production of epoxy alcohols, dihydrodiols, triols and epoxides, including many lipid epoxides associated with resistance. Two epoxide hydrolase genes from Nicotiana benthamiana L., NbEH1.1 and NbEH1.2, were amplified from coding DNA of leaves during a susceptible response to the hemibiotrophic pathogens, Colletotrichum destructivum O’Gara, Colletotrichum orbiculare Berk. and Mont. von Arx. or Pseudomonas syringae pv. tabaci Wolf and Foster, or the hypersensitive resistance response to P. syringae pv. tabaci expressing avrPto. Increases in expression of NbEH1.1 generally occurred during the late biotrophic and necrotrophic stages in the susceptible responses and before the hypersensitive response. NbEH1.2 expression was not significantly induced by C. orbiculare but was induced by C. destructivum, P. syringae pv. tabaci and P. syringae pv. tabaci expressing avrPto, although to a lesser degree than NbEH1.1. Virus-induced gene silencing of NbEH1.1 delayed the appearance of lesions for C. destructivum, reduced populations of P. syringae pv. tabaci and increased populations of P. syringae pv. tabaci expressing avrPto. The importance of epoxide hydrolase during pathogen attack may be related to its roles in detoxification, signalling, or metabolism of antimicrobial compounds.

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 Identification of Arabidopsis Mutants Exhibiting an Altered Hypersensitive Response in Gene-for-Gene Disease Resistance

2000 ◽  
Vol 13 (3) ◽  
pp. 277-286 ◽  
Author(s):  
I-ching Yu ◽  
Kevin A. Fengler ◽  
Steven J. Clough ◽  
Andrew F. Bent
Keyword(s):  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Growth Defects ◽  
Lesion Mimic ◽  
Pathogenesis Related ◽  
Lesion Mimic Mutant ◽  
Mutant Phenotypes ◽  
Temporally Correlated

A mutational study was carried out to isolate Arabidopsis thaliana plants that exhibit full or partial disruption of the RPS2-mediated hypersensitive response (HR) to Pseudomonas syringae that express avrRpt2. Five classes of mutants were identified including mutations at RPS2, dnd mutations causing a “defense, no death” loss-of-HR phenotype, a lesion-mimic mutant that also exhibited an HR¯phenotype, and a number of intermediate or partial-loss-of-HR mutants. Surprisingly, many of these mutants displayed elevated resistance to virulent P. syringae and, in some cases, to Peronospora parasitica. Constitutively elevated levels of pathogenesis-related (PR) gene expression and salicylic acid were also observed. In the lesion-mimic mutant, appearance of elevated resistance was temporally correlated with appearance of lesions. For one of the intermediate lines, resistance was shown to be dependent on elevated levels of salicylic acid. A new locus was identified and named IHR1, after the mutant phenotype of “intermediate HR.” Genetic analysis of the intermediate-HR plant lines was difficult due to uncertainties in distinguishing the partial/intermediate mutant phenotypes from wild type. Despite this difficulty, the intermediate-HR mutants remain of interest because they reveal potential new defense-related loci and because many of these lines exhibit partially elevated disease resistance without dwarfing or other apparent growth defects.

scholarly journals Effector loss drives adaptation of Pseudomonas syringae pv. actinidiae to Actinidia arguta

2021 ◽  
Author(s):  
Lauren M Hemara ◽  
Jay Jayaraman ◽  
Paul Sutherland ◽  
Mirco Montefiori ◽  
Saadiah Arshed ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Durable Resistance ◽  
Host Recognition ◽  
Ion Leakage ◽  
In Planta ◽  
Resistance Response ◽  
Bacterial Pathogenicity ◽  
Effector Triggered Immunity ◽  
Species Specific

A pandemic isolate of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has devastated kiwifruit orchards growing cultivars of Actinidia chinensis. In contrast, A. arguta (kiwiberry) is resistant to Psa3. This resistance is mediated via effector-triggered immunity, as demonstrated by induction of the hypersensitive response in infected A. arguta leaves, observed by microscopy and quantified by ion-leakage assays. Isolates of Psa3 that cause disease in A. arguta have been isolated and analyzed, revealing a 49 kb deletion in the exchangeable effector locus (EEL). This natural EEL-mutant isolate and strains with synthetic knockouts of the EEL were more virulent in A. arguta plantlets than wild-type Psa3. Screening of a complete library of Psa3 effector knockout strains identified increased growth in planta for knockouts of four effectors — AvrRpm1a, HopF1c, HopZ5a, and the EEL effector HopAW1a — suggesting a resistance response in A. arguta. Hypersensitive response (HR) assays indicate that three of these effectors trigger a host species-specific HR. A Psa3 strain with all four effectors knocked out escaped host recognition, but a cumulative increase in bacterial pathogenicity and virulence was not observed. These avirulence effectors can be used in turn to identify the first cognate resistance genes in Actinidia for breeding durable resistance into future kiwifruit cultivars.

scholarly journals CBL-interacting protein kinase 6 negatively regulates immune response to Pseudomonas syringae in Arabidopsis

2017 ◽  
Vol 68 (13) ◽  
pp. 3573-3584 ◽  
Author(s):  
Atish Sardar ◽  
Ashis Kumar Nandi ◽  
Debasis Chattopadhyay
Keyword(s):  
Immune Response ◽  
Protein Kinase ◽  
Pseudomonas Syringae ◽  
Interacting Protein

scholarly journals Natural Variation in the Arabidopsis Response to the Avirulence Gene hopPsyA Uncouples the Hypersensitive Response from Disease Resistance

2005 ◽  
Vol 18 (10) ◽  
pp. 1054-1060 ◽  
Author(s):  
Walter Gassmann
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Plant Disease Resistance ◽  
Natural Variation ◽  
Avirulence Gene ◽  
Tomato Dc3000 ◽  
Recessive Phenotype ◽  
Tight Association ◽  
Gene For Gene

The plant hypersensitive response (HR) is tightly associated with gene-for-gene resistance and has been proposed to function in containing pathogens at the invasion site. This tight association has made it difficult to unequivocally evaluate the importance of HR for plant disease resistance. Here, hopPsyA from Pseudomonas syringae pv. syringae 61 is identified as a new avirulence gene for Arabidopsis that triggers resistance in the absence of macroscopic HR. Resistance to P. syringae pv. tomato DC3000 expressing hopPsyA was EDS1-dependent and NDR1-independent. Intriguingly, several Arabidopsis accessions were resistant to DC3000(hopPsyA) in the absence of HR. This is comparable to the Arabidopsis response to avrRps4, but it is shown that hopPsyA does not signal through RPS4. In a cross between two hopPsyA-resistant accessions that differ in their HR response, the HR segregated as a recessive phenotype regulated by a single locus. This locus, HED1 (HR regulator in EDS1 pathway), is proposed to encode a protein whose activity can cause suppression of the EDS1-dependent HR signaling pathway. HED1-regulated symptomless gene-for-gene resistance responses may explain some cases of Arabidopsis resistance to bacteria that are classified as nonhost resistance.

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.

Early signalling events of autophagy

2013 ◽  
Vol 55 ◽  
pp. 1-15 ◽  
Author(s):  
Laura E. Gallagher ◽  
Edmond Y.W. Chan
Keyword(s):  
Protein Kinase ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Mammalian Cells ◽  
Mammalian Target Of Rapamycin ◽  
Interacting Protein ◽  
The Core ◽  
Autophagy Gene ◽  
Autophagy Induction ◽  
Cellular Pathways

Autophagy is a conserved cellular degradative process important for cellular homoeostasis and survival. An early committal step during the initiation of autophagy requires the actions of a protein kinase called ATG1 (autophagy gene 1). In mammalian cells, ATG1 is represented by ULK1 (uncoordinated-51-like kinase 1), which relies on its essential regulatory cofactors mATG13, FIP200 (focal adhesion kinase family-interacting protein 200 kDa) and ATG101. Much evidence indicates that mTORC1 [mechanistic (also known as mammalian) target of rapamycin complex 1] signals downstream to the ULK1 complex to negatively regulate autophagy. In this chapter, we discuss our understanding on how the mTORC1–ULK1 signalling axis drives the initial steps of autophagy induction. We conclude with a summary of our growing appreciation of the additional cellular pathways that interconnect with the core mTORC1–ULK1 signalling module.

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