RPS2, an Arabidopsis Disease Resistance Locus Specifying Recognition of Pseudomonas syringae Strains Expressing the Avirulence Gene avrRpt2

1993 ◽  
Vol 5 (8) ◽  
pp. 865 ◽  
Author(s):  
Barbara N. Kunkel ◽  
Andrew F. Bent ◽  
Douglas Dahlbeck ◽  
Roger W. Innes ◽  
Brian J. Staskawicz
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Avirulence Gene ◽  
Resistance Locus

scholarly journals RPS2, an Arabidopsis disease resistance locus specifying recognition of Pseudomonas syringae strains expressing the avirulence gene avrRpt2.

1993 ◽  
Vol 5 (8) ◽  
pp. 865-875 ◽  
Author(s):  
B N Kunkel ◽  
A F Bent ◽  
D Dahlbeck ◽  
R W Innes ◽  
B J Staskawicz
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Avirulence Gene ◽  
Resistance Locus

scholarly journals Identification of Three Putative Signal Transduction Genes Involved in R Gene-Specified Disease Resistance in Arabidopsis

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 401-412 ◽  
Author(s):  
Randall F Warren ◽  
Peter M Merritt ◽  
Eric Holub ◽  
Roger W Innes
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Resistance Genes ◽  
Virulent Strain ◽  
Disease Resistance Genes ◽  
Avirulence Gene ◽  
Detectable Effect ◽  
Disease Resistance Gene ◽  
Protein Functions ◽  
Signal Transduction Genes

Abstract The RPS5 disease resistance gene of Arabidopsis mediates recognition of Pseudomonas syringae strains that possess the avirulence gene avrPphB. By screening for loss of RPS5-specified resistance, we identified five pbs (avrPphB susceptible) mutants that represent three different genes. Mutations in PBS1 completely blocked RPS5-mediated resistance, but had little to no effect on resistance specified by other disease resistance genes, suggesting that PBS1 facilitates recognition of the avrPphB protein. The pbs2 mutation dramatically reduced resistance mediated by the RPS5 and RPM1 resistance genes, but had no detectable effect on resistance mediated by RPS4 and had an intermediate effect on RPS2-mediated resistance. The pbs2 mutation also had varying effects on resistance mediated by seven different RPP (recognition of Peronospora parasitica) genes. These data indicate that the PBS2 protein functions in a pathway that is important only to a subset of disease-resistance genes. The pbs3 mutation partially suppressed all four P. syringae-resistance genes (RPS5, RPM1, RPS2, and RPS4), and it had weak-to-intermediate effects on the RPP genes. In addition, the pbs3 mutant allowed higher bacterial growth in response to a virulent strain of P. syringae, indicating that the PBS3 gene product functions in a pathway involved in restricting the spread of both virulent and avirulent pathogens. The pbs mutations are recessive and have been mapped to chromosomes I (pbs2) and V (pbs1 and pbs3).

scholarly journals Mutational Analysis of the Arabidopsis RPS2 Disease Resistance Gene and the Corresponding Pseudomonas syringae avrRpt2 Avirulence Gene

2001 ◽  
Vol 14 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Michael J. Axtell ◽  
Timothy W. McNellis ◽  
Mary Beth Mudgett ◽  
Caroline S. Hsu ◽  
Brian J. Staskawicz
Keyword(s):  
Disease Resistance ◽  
Resistance Gene ◽  
Pseudomonas Syringae ◽  
Resistance Genes ◽  
Mutational Analysis ◽  
Defense Responses ◽  
Avirulence Gene ◽  
Disease Resistance Gene ◽  
In Planta ◽  
Hypersensitive Cell Death

Plants have evolved a large number of disease resistance genes that encode proteins containing conserved structural motifs that function to recognize pathogen signals and to initiate defense responses. The Arabidopsis RPS2 gene encodes a protein representative of the nucleotide-binding site-leucine-rich repeat (NBS-LRR) class of plant resistance proteins. RPS2 specifically recognizes Pseudomonas syringae pv. tomato strains expressing the avrRpt2 gene and initiates defense responses to bacteria carrying avrRpt2, including a hypersensitive cell death response (HR). We present an in planta mutagenesis experiment that resulted in the isolation of a series of rps2 and avrRpt2 alleles that disrupt the RPS2-avrRpt2 gene-for-gene interaction. Seven novel avrRpt2 alleles incapable of eliciting an RPS2-dependent HR all encode proteins with lesions in the C-terminal portion of AvrRpt2 previously shown to be sufficient for RPS2 recognition. Ten novel rps2 alleles were characterized with mutations in the NBS and the LRR. Several of these alleles code for point mutations in motifs that are conserved among NBS-LRR resistance genes, including the third LRR, which suggests the importance of these motifs for resistance gene function.

scholarly journals Soybean resistance genes specific for different Pseudomonas syringae avirulence genes are allelic, or closely linked, at the RPG1 locus.

Genetics ◽  
1995 ◽  
Vol 141 (4) ◽  
pp. 1597-1604 ◽  
Author(s):  
T Ashfield ◽  
N T Keen ◽  
R I Buzzell ◽  
R W Innes
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Resistance Genes ◽  
Disease Resistance Genes ◽  
Avirulence Gene ◽  
Avirulence Genes ◽  
Soybean Resistance

Abstract RPG1 and RPM1 are disease resistance genes in soybean and Arabidopsis, respectively, that confer resistance to Pseudomonas syringae strains expressing the avirulence gene avrB. RPM1 has recently been demonstrated to have a second specificity, also conferring resistance to P. syringae strains expressing avrRpm1. Here we show that alleles, or closely linked genes, exist at the RPG1 locus in soybean that are specific for either avrB or avrRpm1 and thus can distinguish between these two avirulence genes.

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 The Myristylation Motif of Pto Is Not Required for Disease Resistance

1998 ◽  
Vol 11 (6) ◽  
pp. 572-576 ◽  
Author(s):  
Ying-Tsu Loh ◽  
Jianmin Zhou ◽  
Gregory B. Martin
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Cauliflower Mosaic Virus ◽  
Site Directed Mutagenesis ◽  
Avirulence Gene ◽  
35S Promoter ◽  
Wild Type ◽  
Tomato Plants ◽  
Bacterial Speck ◽  
Bacterial Speck Disease

The tomato Pto kinase confers resistance to bacterial speck disease caused by strains of Pseudomonas syringae pv. tomato that express the avirulence gene avrPto. Pto contains a putative myristylation site at its amino terminus that was hypothesized to play a role in localizing Pto in the plant cell. Site-directed mutagenesis was used to change the invariant glycine residue in the myristylation motif to an alanine. Transgenes encoding the mutant Pto(G2A) and wild-type Pto were placed behind the cauliflower mosaic virus 35S promoter and transformed into tomato plants that are susceptible to bacterial speck disease. Both the mutant and wild-type forms of Pto conferred resistance to a strain of P. syringae pv. tomato expressing avrPto. These results indicate that the myristylation motif of Pto is not required for bacterial speck disease resistance.

scholarly journals Molecular mechanisms involved in bacterial speck disease resistance of tomato

1998 ◽  
Vol 353 (1374) ◽  
pp. 1455-1461 ◽  
Author(s):  
Yong–Qiang Gu ◽  
Gregory B. Martin
Keyword(s):  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Plant Defence ◽  
Avirulence Gene ◽  
Physical Interaction ◽  
Bacterial Speck ◽  
Bacterial Speck Disease ◽  
Defence Responses ◽  
Pto Kinase

An important recent advance in the field of plant–microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or nematodes. Disease resistance ( R ) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. The future challenge is to understand how R gene products specifically perceive defence–eliciting signals from the pathogen and transduce those signals to pathways that lead to the activation of plant defence responses. In tomatoes, the Pto kinase (product of the Pto R gene) confers resistance to strains of the bacterial speck pathogen, Pseudomonas syringae pv. tomato , that carry the corresponding avirulence gene avrPto . Resistance to bacterial speck disease is initiated by a mechanism involving the physical interaction of the Pto kinase and the AvrPto protein. This recognition event initiates signalling events that lead to defence responses including an oxidative burst, the hypersensitive response and expression of pathogenesis–related genes. Pto–interacting (Pti) proteins have been identified that appear to act downstream of the Pto kinase and our current studies are directed at elucidating the roles of these components.

Comparative Mapping of Three Bacterial, Three Fungal, and One Virus Disease-resistance Genes in Common Bean

HortScience ◽  
1998 ◽  
Vol 33 (3) ◽  
pp. 547a-547
Author(s):  
Geunhwa Jung ◽  
James Nienhuis ◽  
Dermot P. Coyne ◽  
H.M. Ariyarathne
Keyword(s):  
Disease Resistance ◽  
Common Bean ◽  
Pseudomonas Syringae ◽  
Resistance Genes ◽  
Fungal Pathogens ◽  
Xanthomonas Campestris ◽  
Virus Disease ◽  
Disease Resistance Genes ◽  
Brown Spot ◽  
Viral Pathogen

Common bacterial blight (CBB), bacterial brown spot (BBS), and halo blight (HB), incited by the bacterial pathogens Xanthomonas campestris pv. phaseoli (Smith) Dye, Pseodomonas syringae pv. syringa, and Pseudomonas syringae pv. phaseolicola, respectively are important diseases of common bean. In addition three fungal pathogens, web blight (WB) Thanatephorus cucumeris, rust Uromyces appendiculatus, and white mold (WM) Sclerotinia sclerotiorum, are also destructive diseases attacking common bean. Bean common mosaic virus is also one of most major virus disease. Resistance genes (QTLs and major genes) to three bacterial (CBB, BBS, and HB), three fungal (WB, rust, and WM), and one viral pathogen (BCMV) were previously mapped in two common bean populations (BAC 6 × HT 7719 and Belneb RR-1 × A55). The objective of this research was to use an integrated RAPD map of the two populations to compare the positions and effect of resistance QTL in common bean. Results indicate that two chromosomal regions associated with QTL for CBB resistance mapped in both populations. The same chromosomal regions associated with QTL for disease resistance to different pathogens or same pathogens were detected in the integrated population.

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 Uncoupling Salicylic Acid-Dependent Cell Death and Defense-Related Responses From Disease Resistance in the Arabidopsis Mutant acd5

Genetics ◽  
2000 ◽  
Vol 156 (1) ◽  
pp. 341-350
Author(s):  
Jean T Greenberg ◽  
F Paul Silverman ◽  
Hua Liang
Keyword(s):  
Cell Death ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Higher Plants ◽  
Ethylene Signaling ◽  
Symptom Development ◽  
Wild Type ◽  
Dependent Cell ◽  
Arabidopsis Mutant

Abstract Salicylic acid (SA) is required for resistance to many diseases in higher plants. SA-dependent cell death and defense-related responses have been correlated with disease resistance. The accelerated cell death 5 mutant of Arabidopsis provides additional genetic evidence that SA regulates cell death and defense-related responses. However, in acd5, these events are uncoupled from disease resistance. acd5 plants are more susceptible to Pseudomonas syringae early in development and show spontaneous SA accumulation, cell death, and defense-related markers later in development. In acd5 plants, cell death and defense-related responses are SA dependent but they do not confer disease resistance. Double mutants with acd5 and nonexpressor of PR1, in which SA signaling is partially blocked, show greatly attenuated cell death, indicating a role for NPR1 in controlling cell death. The hormone ethylene potentiates the effects of SA and is important for disease symptom development in Arabidopsis. Double mutants of acd5 and ethylene insensitive 2, in which ethylene signaling is blocked, show decreased cell death, supporting a role for ethylene in cell death control. We propose that acd5 plants mimic P. syringae-infected wild-type plants and that both SA and ethylene are normally involved in regulating cell death during some susceptible pathogen infections.

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