A disease resistance gene in Arabidopsis with specificity for two different pathogen avirulence genes.

Bisgrove, Sherryl R.; Simonich, Michael T.; Smith, Nadine M.; Sattler, Airlie; Innes, Roger W.

doi:10.1105/tpc.6.7.927

Cited by 242 publications

(134 citation statements)

References 21 publications

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“…The Arabidopsis RIN4 protein is thought to serve as a guardee for RPM1, which presumably monitors the AvrB-mediated phosphorylation of RIN4 to induce resistance signaling. The lack of sequence conservation between RPM1 and RPG1-B indicates independent evolution of the two R proteins, in spite of their shared specificity for the same avirulence effector (Bisgrove et al, 1994;Grant et al, 1995;Ashfield et al, 2004). This is supported by the differences in their requirements for signaling components.…”

Section: Discussionmentioning

confidence: 63%

RPG1-B-Derived Resistance to AvrB-Expressing Pseudomonas syringae Requires RIN4-Like Proteins in Soybean

Selote

Kachroo

2010

Plant Physiology

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Soybean (Glycine max) RPG1-B (for resistance to Pseudomonas syringae pv glycinea) mediates species-specific resistance to P. syringae expressing the avirulence protein AvrB, similar to the nonorthologous RPM1 in Arabidopsis (Arabidopsis thaliana). RPM1-derived signaling is presumably induced upon AvrB-derived modification of the RPM1-interacting protein, RIN4 (for RPM1-interacting 4). We show that, similar to RPM1, RPG1-B does not directly interact with AvrB but associates with RIN4-like proteins from soybean. Unlike Arabidopsis, soybean contains at least four RIN4-like proteins (GmRIN4a to GmRIN4d). GmRIN4b, but not GmRIN4a, complements the Arabidopsis rin4 mutation. Both GmRIN4a and GmRIN4b bind AvrB, but only GmRIN4b binds RPG1-B. Silencing either GmRIN4a or GmRIN4b abrogates RPG1-B-derived resistance to P. syringae expressing AvrB. Binding studies show that GmRIN4b interacts with GmRIN4a as well as with two other AvrB/RPG1-B-interacting isoforms, GmRIN4c and GmRIN4d. The lack of functional redundancy among GmRIN4a and GmRIN4b and their abilities to interact with each other suggest that the two proteins might function as a heteromeric complex in mediating RPG1-B-derived resistance. Silencing GmRIN4a or GmRIN4b in rpg1-b plants enhances basal resistance to virulent strains of P. syringae and the oomycete Phytophthora sojae. Interestingly, GmRIN4a- or GmRIN4b-silenced rpg1-b plants respond differently to AvrB-expressing bacteria. Although both GmRIN4a and GmRIN4b function to monitor AvrB in the presence of RPG1-B, GmRIN4a, but not GmRIN4b, negatively regulates AvrB virulence activity in the absence of RPG1-B.

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Section: Discussionmentioning

confidence: 63%

RPG1-B-Derived Resistance to AvrB-Expressing Pseudomonas syringae Requires RIN4-Like Proteins in Soybean

Selote

Kachroo

2010

Plant Physiology

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“…Leaf inoculation of accession Columbia-0 (Col-0), which carries the Rpm1 resistance gene with Psm expressing the avirulence gene AvrRpm1 (Psm avrRpm1), by contrast, elicits an HR associated with rapid cell death at inoculation sites (Bisgrove et al, 1994;Delledonne et al, 1998). Early defense responses associated with the HR do not fully abrogate but significantly restrict bacterial multiplication.…”

Section: Resultsmentioning

confidence: 99%

Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

et al. 2009

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Systemic acquired resistance (SAR) develops in response to local microbial leaf inoculation and renders the whole plant more resistant to subsequent pathogen infection. Accumulation of salicylic acid (SA) in noninfected plant parts is required for SAR, and methyl salicylate (MeSA) and jasmonate (JA) are proposed to have critical roles during SAR long-distance signaling from inoculated to distant leaves. Here, we address the significance of MeSA and JA during SAR development in Arabidopsis thaliana. MeSA production increases in leaves inoculated with the SAR-inducing bacterial pathogen Pseudomonas syringae; however, most MeSA is emitted into the atmosphere, and only small amounts are retained. We show that in several Arabidopsis defense mutants, the abilities to produce MeSA and to establish SAR do not coincide. T-DNA insertion lines defective in expression of a pathogen-responsive SA methyltransferase gene are completely devoid of induced MeSA production but increase systemic SA levels and develop SAR upon local P. syringae inoculation. Therefore, MeSA is dispensable for SAR in Arabidopsis, and SA accumulation in distant leaves appears to occur by de novo synthesis via isochorismate synthase. We show that MeSA production induced by P. syringae depends on the JA pathway but that JA biosynthesis or downstream signaling is not required for SAR. In compatible interactions, MeSA production depends on the P. syringae virulence factor coronatine, suggesting that the phytopathogen uses coronatine-mediated volatilization of MeSA from leaves to attenuate the SA-based defense pathway.

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“…Common genetic background for all examined mutants is accession Col (Col-0 for cry1cry2 and phyAphyB; Col-3 for phot1phot2), implicating that each line harbors the resistance gene Rpm1 whose product recognizes the bacterial avirulence protein AvrRpm1. This recognition event is causative for the Psm avrRpm1-induced HR and early SA accumulation in wild-type Col (Bisgrove et al, 1994;Mishina et al, 2008).…”

Section: Photoreceptor Signaling Only Moderately Affects Induction Ofmentioning

confidence: 99%

Light Regulation and Daytime Dependency of Inducible Plant Defenses in Arabidopsis: Phytochrome Signaling Controls Systemic Acquired Resistance Rather Than Local Defense

2008

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We have examined molecular and physiological principles underlying the light dependency of defense activation in Arabidopsis (Arabidopsis thaliana) plants challenged with the bacterial pathogen Pseudomonas syringae. Within a fixed light/dark cycle, plant defense responses and disease resistance significantly depend on the time of day when pathogen contact takes place. Morning and midday inoculations result in higher salicylic acid accumulation, faster expression of pathogenesis-related genes, and a more pronounced hypersensitive response than inoculations in the evening or at night. Rather than to the plants' circadian rhythm, this increased plant defense capability upon day inoculations is attributable to the availability of a prolonged light period during the early plant-pathogen interaction. Moreover, pathogen responses of Arabidopsis double mutants affected in light perception, i.e. cryptochrome1cryptochrome2 (cry1cry2), phototropin1phototropin2 (phot1phot2), and phytochromeAphytochromeB (phyAphyB) were assessed. Induction of defense responses by either avirulent or virulent P. syringae at inoculation sites is relatively robust in leaves of photoreceptor mutants, indicating little cross talk between local defense and light signaling. In addition, the blue-light receptor mutants cry1cry2 and phot1phot2 are both capable of establishing a full systemic acquired resistance (SAR) response. Induction of SAR and salicylic-acid-dependent systemic defense reactions, however, are compromised in phyAphyB mutants. Phytochrome regulation of SAR involves the essential SAR component FLAVIN-DEPENDENT MONOOXYGENASE1. Our findings highlight the importance of phytochrome photoperception during systemic rather than local resistance induction. The phytochrome system seems to accommodate the supply of light energy to the energetically costly increase in whole plant resistance.

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A disease resistance gene in Arabidopsis with specificity for two different pathogen avirulence genes.

Cited by 242 publications

References 21 publications

RPG1-B-Derived Resistance to AvrB-Expressing Pseudomonas syringae Requires RIN4-Like Proteins in Soybean

RPG1-B-Derived Resistance to AvrB-Expressing Pseudomonas syringae Requires RIN4-Like Proteins in Soybean

Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis

Light Regulation and Daytime Dependency of Inducible Plant Defenses in Arabidopsis: Phytochrome Signaling Controls Systemic Acquired Resistance Rather Than Local Defense

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