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Specific missense alleles of the arabidopsis jasmonic acid co-receptor COI1 regulate innate immune receptor accumulation and function.

He Y, Chung EH, Hubert DA, Tornero P, Dangl JL - PLoS Genet. (2012)

Bottom Line: The first, also observed in coi1-1 allele, includes enhanced basal defense against the virulent bacterial pathogen Pto DC3000 and enhanced effector-triggered immunity (ETI) mediated by the NB-LRR RPM1 protein in both rar1 and wild-type backgrounds.These results suggest that the coi1(rsp) proteins regulate NB-LRR protein accumulation independent of JA signaling.Together, our data demonstrate a role for COI1 in disease resistance independent of JA signaling and provide a molecular link between the JA and NB-LRR signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

ABSTRACT
Plants utilize proteins containing nucleotide binding site (NB) and leucine-rich repeat (LRR) domains as intracellular innate immune receptors to recognize pathogens and initiate defense responses. Since mis-activation of defense responses can lead to tissue damage and even developmental arrest, proper regulation of NB-LRR protein signaling is critical. RAR1, SGT1, and HSP90 act as regulatory chaperones of pre-activation NB-LRR steady-state proteins. We extended our analysis of mutants derived from a rar1 suppressor screen and present two allelic rar1 suppressor (rsp) mutations of Arabidopsis COI1. Like all other coi1 mutations, coi1(rsp) missense mutations impair Jasmonic Acid (JA) signaling resulting in JA-insensitivity. However, unlike previously identified coi1 alleles, both coi1(rsp) alleles lack a male sterile phenotype. The coi1(rsp) mutants express two sets of disease resistance phenotypes. The first, also observed in coi1-1 allele, includes enhanced basal defense against the virulent bacterial pathogen Pto DC3000 and enhanced effector-triggered immunity (ETI) mediated by the NB-LRR RPM1 protein in both rar1 and wild-type backgrounds. These enhanced disease resistance phenotypes depend on the JA signaling function of COI1. Additionally, the coi1(rsp) mutants showed a unique inability to properly regulate RPM1 accumulation and HR, exhibited increased RPM1 levels in rar1, and weakened RPM1-mediated HR in RAR1. Importantly, there was no change in the steady-state levels or HR function of RPM1 in coi1-1. These results suggest that the coi1(rsp) proteins regulate NB-LRR protein accumulation independent of JA signaling. Based on the phenotypic similarities and genetic interactions among coi1(rsp), sgt1b, and hsp90.2(rsp) mutants, our data suggest that COI1 affects NB-LRR accumulation via two NB-LRR co-chaperones, SGT1b and HSP90. Together, our data demonstrate a role for COI1 in disease resistance independent of JA signaling and provide a molecular link between the JA and NB-LRR signaling pathways.

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coi1rsp alleles exhibit enhanced basal defense and additionally weakly suppress RPM1 HR function.(A–B) Bacterial growth analysis of Pto DC3000(EV) (A) and Pto DC3000(avrRpm1) (B). Bacteria were hand-infiltrated into leaves of each indicated genotype and counted at day 0 and day 3. Error bars represent 2× SE. Pairwise comparisons for all means for bacterial growth on day 3 were performed with One-Way ANOVA test followed by Tukey-Kramer HSD at 95% confidence limits. (C) Conductivity measurements after inoculation with high concentration Pto DC3000(avrRpm1) (5×107 cfu/ml). Error bars represent 2× SE. The pathogen growth and HR assays were performed independently a minimum of three times with similar results.
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pgen-1003018-g004: coi1rsp alleles exhibit enhanced basal defense and additionally weakly suppress RPM1 HR function.(A–B) Bacterial growth analysis of Pto DC3000(EV) (A) and Pto DC3000(avrRpm1) (B). Bacteria were hand-infiltrated into leaves of each indicated genotype and counted at day 0 and day 3. Error bars represent 2× SE. Pairwise comparisons for all means for bacterial growth on day 3 were performed with One-Way ANOVA test followed by Tukey-Kramer HSD at 95% confidence limits. (C) Conductivity measurements after inoculation with high concentration Pto DC3000(avrRpm1) (5×107 cfu/ml). Error bars represent 2× SE. The pathogen growth and HR assays were performed independently a minimum of three times with similar results.

Mentions: We introduced the coi1rsp alleles into an isogenic RAR1 background using marker-assisted breeding (see Methods). To further study the role of COI1 in regulating RPM1 function, we inoculated both coi1rsp alleles, coi1-1 and coi1-16 plants with Pto DC3000(avrRpm1) and measured bacterial growth (Figure 4B). The coi1rsp and coi1-16 mutants were as resistant as wild type. The coi1-1 mutant displayed slightly enhanced resistance compared with wild type. We also measured RPM1-mediated HR in these coi1 single mutants using the ion leakage assay (Figure 4C). Surprisingly, both coi1rsp alleles weakly suppressed RPM1-mediated HR. We crossed RPM1-myc into these coi1rsp, coi1-1 and coi1-16 single mutants and measured RPM1-myc protein levels (Figure 3C). We observed no obvious changes in RPM1-myc levels in any of the single coi1 mutant. We conclude from these data that coi1rsp mutations differentially regulate RPM1 function in rar1 or RAR1 backgrounds.


Specific missense alleles of the arabidopsis jasmonic acid co-receptor COI1 regulate innate immune receptor accumulation and function.

He Y, Chung EH, Hubert DA, Tornero P, Dangl JL - PLoS Genet. (2012)

coi1rsp alleles exhibit enhanced basal defense and additionally weakly suppress RPM1 HR function.(A–B) Bacterial growth analysis of Pto DC3000(EV) (A) and Pto DC3000(avrRpm1) (B). Bacteria were hand-infiltrated into leaves of each indicated genotype and counted at day 0 and day 3. Error bars represent 2× SE. Pairwise comparisons for all means for bacterial growth on day 3 were performed with One-Way ANOVA test followed by Tukey-Kramer HSD at 95% confidence limits. (C) Conductivity measurements after inoculation with high concentration Pto DC3000(avrRpm1) (5×107 cfu/ml). Error bars represent 2× SE. The pathogen growth and HR assays were performed independently a minimum of three times with similar results.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC3475666&req=5

pgen-1003018-g004: coi1rsp alleles exhibit enhanced basal defense and additionally weakly suppress RPM1 HR function.(A–B) Bacterial growth analysis of Pto DC3000(EV) (A) and Pto DC3000(avrRpm1) (B). Bacteria were hand-infiltrated into leaves of each indicated genotype and counted at day 0 and day 3. Error bars represent 2× SE. Pairwise comparisons for all means for bacterial growth on day 3 were performed with One-Way ANOVA test followed by Tukey-Kramer HSD at 95% confidence limits. (C) Conductivity measurements after inoculation with high concentration Pto DC3000(avrRpm1) (5×107 cfu/ml). Error bars represent 2× SE. The pathogen growth and HR assays were performed independently a minimum of three times with similar results.
Mentions: We introduced the coi1rsp alleles into an isogenic RAR1 background using marker-assisted breeding (see Methods). To further study the role of COI1 in regulating RPM1 function, we inoculated both coi1rsp alleles, coi1-1 and coi1-16 plants with Pto DC3000(avrRpm1) and measured bacterial growth (Figure 4B). The coi1rsp and coi1-16 mutants were as resistant as wild type. The coi1-1 mutant displayed slightly enhanced resistance compared with wild type. We also measured RPM1-mediated HR in these coi1 single mutants using the ion leakage assay (Figure 4C). Surprisingly, both coi1rsp alleles weakly suppressed RPM1-mediated HR. We crossed RPM1-myc into these coi1rsp, coi1-1 and coi1-16 single mutants and measured RPM1-myc protein levels (Figure 3C). We observed no obvious changes in RPM1-myc levels in any of the single coi1 mutant. We conclude from these data that coi1rsp mutations differentially regulate RPM1 function in rar1 or RAR1 backgrounds.

Bottom Line: The first, also observed in coi1-1 allele, includes enhanced basal defense against the virulent bacterial pathogen Pto DC3000 and enhanced effector-triggered immunity (ETI) mediated by the NB-LRR RPM1 protein in both rar1 and wild-type backgrounds.These results suggest that the coi1(rsp) proteins regulate NB-LRR protein accumulation independent of JA signaling.Together, our data demonstrate a role for COI1 in disease resistance independent of JA signaling and provide a molecular link between the JA and NB-LRR signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Biology, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

ABSTRACT
Plants utilize proteins containing nucleotide binding site (NB) and leucine-rich repeat (LRR) domains as intracellular innate immune receptors to recognize pathogens and initiate defense responses. Since mis-activation of defense responses can lead to tissue damage and even developmental arrest, proper regulation of NB-LRR protein signaling is critical. RAR1, SGT1, and HSP90 act as regulatory chaperones of pre-activation NB-LRR steady-state proteins. We extended our analysis of mutants derived from a rar1 suppressor screen and present two allelic rar1 suppressor (rsp) mutations of Arabidopsis COI1. Like all other coi1 mutations, coi1(rsp) missense mutations impair Jasmonic Acid (JA) signaling resulting in JA-insensitivity. However, unlike previously identified coi1 alleles, both coi1(rsp) alleles lack a male sterile phenotype. The coi1(rsp) mutants express two sets of disease resistance phenotypes. The first, also observed in coi1-1 allele, includes enhanced basal defense against the virulent bacterial pathogen Pto DC3000 and enhanced effector-triggered immunity (ETI) mediated by the NB-LRR RPM1 protein in both rar1 and wild-type backgrounds. These enhanced disease resistance phenotypes depend on the JA signaling function of COI1. Additionally, the coi1(rsp) mutants showed a unique inability to properly regulate RPM1 accumulation and HR, exhibited increased RPM1 levels in rar1, and weakened RPM1-mediated HR in RAR1. Importantly, there was no change in the steady-state levels or HR function of RPM1 in coi1-1. These results suggest that the coi1(rsp) proteins regulate NB-LRR protein accumulation independent of JA signaling. Based on the phenotypic similarities and genetic interactions among coi1(rsp), sgt1b, and hsp90.2(rsp) mutants, our data suggest that COI1 affects NB-LRR accumulation via two NB-LRR co-chaperones, SGT1b and HSP90. Together, our data demonstrate a role for COI1 in disease resistance independent of JA signaling and provide a molecular link between the JA and NB-LRR signaling pathways.

Show MeSH
Related in: MedlinePlus