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NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants.

Fu ZQ, Yan S, Saleh A, Wang W, Ruble J, Oka N, Mohan R, Spoel SH, Tada Y, Zheng N, Dong X - Nature (2012)

Bottom Line: Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance.Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity.Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Department of Biology, PO Box 90338, Duke University, Durham, North Carolina 27708, USA.

ABSTRACT
Salicylic acid (SA) is a plant immune signal produced after pathogen challenge to induce systemic acquired resistance. It is the only major plant hormone for which the receptor has not been firmly identified. Systemic acquired resistance in Arabidopsis requires the transcription cofactor nonexpresser of PR genes 1 (NPR1), the degradation of which acts as a molecular switch. Here we show that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as adaptors of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in an SA-regulated manner. Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance. Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity. Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

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SA receptors control NPR1 stability to regulate SAR and ETIa, SAR test in WT, npr3, npr4, npr3 npr4 (npr34), npr1 npr3 npr4 (npr134), and npr1. b-d, ETI test in different mutants using Psm ES4326/avrRpt2. b, The hypersensitive response phenotype 2 and 3 days post inoculation (dpi). c, Ion leakage measurement. Error bars represent SD (n=4). d, Growth of Psm ES4326/avrRpt2. In a and d, Error bars represent 95% confidence intervals (n=6-8). cfu, colony forming units. *, P<0.05; ***, P<0.001. e-g, Close-up images of an infection site by Psm ES4326/avrRpt2. Yellow colour in g and h indicates dead cells and green colour indicates npr1C82A-GFP. Arrows point to intact cells inside the inoculated area. h, Image of the whole infection site showing high npr1C82A-GFP accumulation surrounding the PCD zone. The rectangle shows the area from which the close-up images in e-g were taken.
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Figure 4: SA receptors control NPR1 stability to regulate SAR and ETIa, SAR test in WT, npr3, npr4, npr3 npr4 (npr34), npr1 npr3 npr4 (npr134), and npr1. b-d, ETI test in different mutants using Psm ES4326/avrRpt2. b, The hypersensitive response phenotype 2 and 3 days post inoculation (dpi). c, Ion leakage measurement. Error bars represent SD (n=4). d, Growth of Psm ES4326/avrRpt2. In a and d, Error bars represent 95% confidence intervals (n=6-8). cfu, colony forming units. *, P<0.05; ***, P<0.001. e-g, Close-up images of an infection site by Psm ES4326/avrRpt2. Yellow colour in g and h indicates dead cells and green colour indicates npr1C82A-GFP. Arrows point to intact cells inside the inoculated area. h, Image of the whole infection site showing high npr1C82A-GFP accumulation surrounding the PCD zone. The rectangle shows the area from which the close-up images in e-g were taken.

Mentions: To understand the biological significance of NPR3/4-mediated degradation of NPR1, a positive regulator of SAR, we first performed SAR tests in the npr3, npr4 and npr3 npr4 mutants using Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326). Consistent with a previous report11, there was a significant reduction in Psm ES4326 growth in the npr3 npr4 double mutant without SAR induction (Fig. 4a). However, even after SAR induction by local inoculation of avirulent Psm ES4326/avrRpt2, no further reduction in growth of virulent Psm ES4326 in systemic tissue was observed in the npr3 npr4 double mutant. To a lesser degree, SAR was also defective in the npr3 single mutant. Thus, stabilization of NPR1 protein in the npr3, and npr3 npr4 mutants rendered these plants insensitive to SAR induction. This phenotype is similar to that observed in the cul3a cul3b double mutant10, validating the role of NPR3 and NPR4 in CUL3-mediated degradation of NPR1 and SAR.


NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants.

Fu ZQ, Yan S, Saleh A, Wang W, Ruble J, Oka N, Mohan R, Spoel SH, Tada Y, Zheng N, Dong X - Nature (2012)

SA receptors control NPR1 stability to regulate SAR and ETIa, SAR test in WT, npr3, npr4, npr3 npr4 (npr34), npr1 npr3 npr4 (npr134), and npr1. b-d, ETI test in different mutants using Psm ES4326/avrRpt2. b, The hypersensitive response phenotype 2 and 3 days post inoculation (dpi). c, Ion leakage measurement. Error bars represent SD (n=4). d, Growth of Psm ES4326/avrRpt2. In a and d, Error bars represent 95% confidence intervals (n=6-8). cfu, colony forming units. *, P<0.05; ***, P<0.001. e-g, Close-up images of an infection site by Psm ES4326/avrRpt2. Yellow colour in g and h indicates dead cells and green colour indicates npr1C82A-GFP. Arrows point to intact cells inside the inoculated area. h, Image of the whole infection site showing high npr1C82A-GFP accumulation surrounding the PCD zone. The rectangle shows the area from which the close-up images in e-g were taken.
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Figure 4: SA receptors control NPR1 stability to regulate SAR and ETIa, SAR test in WT, npr3, npr4, npr3 npr4 (npr34), npr1 npr3 npr4 (npr134), and npr1. b-d, ETI test in different mutants using Psm ES4326/avrRpt2. b, The hypersensitive response phenotype 2 and 3 days post inoculation (dpi). c, Ion leakage measurement. Error bars represent SD (n=4). d, Growth of Psm ES4326/avrRpt2. In a and d, Error bars represent 95% confidence intervals (n=6-8). cfu, colony forming units. *, P<0.05; ***, P<0.001. e-g, Close-up images of an infection site by Psm ES4326/avrRpt2. Yellow colour in g and h indicates dead cells and green colour indicates npr1C82A-GFP. Arrows point to intact cells inside the inoculated area. h, Image of the whole infection site showing high npr1C82A-GFP accumulation surrounding the PCD zone. The rectangle shows the area from which the close-up images in e-g were taken.
Mentions: To understand the biological significance of NPR3/4-mediated degradation of NPR1, a positive regulator of SAR, we first performed SAR tests in the npr3, npr4 and npr3 npr4 mutants using Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326). Consistent with a previous report11, there was a significant reduction in Psm ES4326 growth in the npr3 npr4 double mutant without SAR induction (Fig. 4a). However, even after SAR induction by local inoculation of avirulent Psm ES4326/avrRpt2, no further reduction in growth of virulent Psm ES4326 in systemic tissue was observed in the npr3 npr4 double mutant. To a lesser degree, SAR was also defective in the npr3 single mutant. Thus, stabilization of NPR1 protein in the npr3, and npr3 npr4 mutants rendered these plants insensitive to SAR induction. This phenotype is similar to that observed in the cul3a cul3b double mutant10, validating the role of NPR3 and NPR4 in CUL3-mediated degradation of NPR1 and SAR.

Bottom Line: Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance.Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity.Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

View Article: PubMed Central - PubMed

Affiliation: Howard Hughes Medical Institute-Gordon and Betty Moore Foundation, Department of Biology, PO Box 90338, Duke University, Durham, North Carolina 27708, USA.

ABSTRACT
Salicylic acid (SA) is a plant immune signal produced after pathogen challenge to induce systemic acquired resistance. It is the only major plant hormone for which the receptor has not been firmly identified. Systemic acquired resistance in Arabidopsis requires the transcription cofactor nonexpresser of PR genes 1 (NPR1), the degradation of which acts as a molecular switch. Here we show that the NPR1 paralogues NPR3 and NPR4 are SA receptors that bind SA with different affinities. NPR3 and NPR4 function as adaptors of the Cullin 3 ubiquitin E3 ligase to mediate NPR1 degradation in an SA-regulated manner. Accordingly, the Arabidopsis npr3 npr4 double mutant accumulates higher levels of NPR1, and is insensitive to induction of systemic acquired resistance. Moreover, this mutant is defective in pathogen effector-triggered programmed cell death and immunity. Our study reveals the mechanism of SA perception in determining cell death and survival in response to pathogen challenge.

Show MeSH
Related in: MedlinePlus