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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 are insensitive to JA.(A) Seedlings of the indicated genotypes were grown on MS medium (control) or medium containing 10 or 50 µM MeJA. (B) Inhibition of root elongation by 50 µM MeJA in at least twenty seedlings of indicated genotypes. This assay was performed independently three times with similar results.
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pgen-1003018-g005: coi1rsp alleles are insensitive to JA.(A) Seedlings of the indicated genotypes were grown on MS medium (control) or medium containing 10 or 50 µM MeJA. (B) Inhibition of root elongation by 50 µM MeJA in at least twenty seedlings of indicated genotypes. This assay was performed independently three times with similar results.

Mentions: COI1 has an essential role in JA signaling; all previously isolated COI1 mutations caused insensitivity to JA-mediated inhibition of seedling growth [32], [43], [45]. We compared JA-insensitivity phenotypes of the coi1rsp alleles to coi1-1 using a growth inhibition assay where plants were grown in the presence of MeJA, a functional JA derivative (Figure 5). Like coi1-1, the MeJA-treated coi1rsp seedlings grew on MeJA-containing media, while the growth of wild type seedlings was severely inhibited (Figure 5A). MeJA treated coi1rsp seedlings were clearly smaller than the untreated seedlings, suggesting that the coi1rsp alleles are not as insensitive to JA as coi1-1. We quantified these phenotypes with a root elongation assay (Figure 5B). The allele coi1-1 displayed root growth inhibition of only about 14% in the presence of 50 µM MeJA. Compared with coi1-1, coi1-16 and both coi1rsp alleles displayed intermediate insensitivity to MeJA treatment. Their root growth was inhibited about 27%, 30% and 42% respectively, while the root growth inhibition was more than 60% in wild type seedlings. Thus, the coi1rsp alleles are JA-insensitive.


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 are insensitive to JA.(A) Seedlings of the indicated genotypes were grown on MS medium (control) or medium containing 10 or 50 µM MeJA. (B) Inhibition of root elongation by 50 µM MeJA in at least twenty seedlings of indicated genotypes. This assay was performed independently three times with similar results.
© Copyright Policy
Related In: Results  -  Collection

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

pgen-1003018-g005: coi1rsp alleles are insensitive to JA.(A) Seedlings of the indicated genotypes were grown on MS medium (control) or medium containing 10 or 50 µM MeJA. (B) Inhibition of root elongation by 50 µM MeJA in at least twenty seedlings of indicated genotypes. This assay was performed independently three times with similar results.
Mentions: COI1 has an essential role in JA signaling; all previously isolated COI1 mutations caused insensitivity to JA-mediated inhibition of seedling growth [32], [43], [45]. We compared JA-insensitivity phenotypes of the coi1rsp alleles to coi1-1 using a growth inhibition assay where plants were grown in the presence of MeJA, a functional JA derivative (Figure 5). Like coi1-1, the MeJA-treated coi1rsp seedlings grew on MeJA-containing media, while the growth of wild type seedlings was severely inhibited (Figure 5A). MeJA treated coi1rsp seedlings were clearly smaller than the untreated seedlings, suggesting that the coi1rsp alleles are not as insensitive to JA as coi1-1. We quantified these phenotypes with a root elongation assay (Figure 5B). The allele coi1-1 displayed root growth inhibition of only about 14% in the presence of 50 µM MeJA. Compared with coi1-1, coi1-16 and both coi1rsp alleles displayed intermediate insensitivity to MeJA treatment. Their root growth was inhibited about 27%, 30% and 42% respectively, while the root growth inhibition was more than 60% in wild type seedlings. Thus, the coi1rsp alleles are JA-insensitive.

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