A critical role of two positively charged amino acids in the Jas motif of Arabidopsis JAZ proteins in mediating coronatine‐ and jasmonoyl isoleucine‐dependent interactions with the COI1 F‐box protein

Melotto, Maeli; Mecey, Christy; Niu, Yajie; Chung, Hoo Sun; Katsir, Leron; Yao, Jian; Zeng, Weiqing; Thines, Bryan; Staswick, Paul E.; Browse, John; Howe, Gregg A.; He, Sheng Yang

doi:10.1111/j.1365-313x.2008.03566.x

Cited by 331 publications

(384 citation statements)

References 31 publications

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“…Coronatine is a phytotoxin produced by several P. syringae pathovars, including Psm and P. syringae pv tomato DC3000 (Pst; Bender et al, 1999). It acts as a bacterial virulence factor that counteracts SA-dependent plant defense reactions by acting as a structural and functional mimic of bioactive jasmonates, most notably JA-Ile (Brooks et al, 2005;Thines et al, 2007;Katsir et al, 2008;Melotto et al, 2008). The availability of coronatine-deficient (cor 2 ) Pst mutants (Brooks et al, 2004) allowed us to test whether P. syringae-induced MeSA production would require the action of coronatine.…”

Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

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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Section: Ja Signaling Regulates Mesa Production But Not Sarmentioning

confidence: 99%

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

et al. 2009

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“…The Jas motif is important for interactions with COI1, the MYC transcription factors, and EIN3/EIL1 (Melotto et al, 2008;Chini et al, 2009;Zhu et al, 2011) and is required for JAZ protein breakdown upon perception of JA-Ile ). In line with this, ectopically expressed JAZ proteins that lack the Jas domain are not targeted for proteasome-mediated degradation, resulting in a strong JAinsensitive phenotype .…”

Section: Introductionmentioning

confidence: 99%

Salicylic Acid Suppresses Jasmonic Acid Signaling Downstream of SCFCOI1-JAZ by Targeting GCC Promoter Motifs via Transcription Factor ORA59

et al. 2013

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Antagonism between the defense hormones salicylic acid (SA) and jasmonic acid (JA) plays a central role in the modulation of the plant immune signaling network, but the molecular mechanisms underlying this phenomenon are largely unknown. Here, we demonstrate that suppression of the JA pathway by SA functions downstream of the E3 ubiquitin-ligase Skip-Cullin-F-box complex SCF COI1 , which targets JASMONATE ZIM-domain transcriptional repressor proteins (JAZs) for proteasomemediated degradation. In addition, neither the stability nor the JA-induced degradation of JAZs was affected by SA. In silico promoter analysis of the SA/JA crosstalk transcriptome revealed that the 1-kb promoter regions of JA-responsive genes that are suppressed by SA are significantly enriched in the JA-responsive GCC-box motifs. Using GCC:GUS lines carrying four copies of the GCC-box fused to the b-glucuronidase reporter gene, we showed that the GCC-box motif is sufficient for SA-mediated suppression of JA-responsive gene expression. Using plants overexpressing the GCC-box binding APETALA2/ETHYLENE RESPONSE FACTOR (AP2/ERF) transcription factors ERF1 or ORA59, we found that SA strongly reduces the accumulation of ORA59 but not that of ERF1. Collectively, these data indicate that the SA pathway inhibits JA signaling downstream of the SCF COI1 -JAZ complex by targeting GCC-box motifs in JA-responsive promoters via a negative effect on the transcriptional activator ORA59.

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“…JA-Ile and to a lesser extent other amino acid conjugated forms of JA, but not JA, MeJA or OPDA, promote the interaction between COI1 and repressors of the JA signal known as jasmonate ZIM-domain (JAZ) proteins. This interaction leads to the subsequent ubiquitin-mediated degradation of JAZ proteins (Chini et al, 2007;Thines et al, 2007;Katsir et al, 2008b;Melotto et al, 2008). COR shows structural similarity to JA-Ile (reviewed in Staswick, 2008), and acts as a potent agonist of this system.…”

Section: Introductionmentioning

confidence: 99%

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

Thatcher

Manners

Kazan³

2009

The Plant Journal

265

298

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SUMMARYAlthough defense responses mediated by the plant oxylipin jasmonic acid (JA) are often necessary for resistance against pathogens with necrotrophic lifestyles, in this report we demonstrate that jasmonate signaling mediated through COI1 in Arabidopsis thaliana is responsible for susceptibility to wilt disease caused by the root-infecting fungal pathogen Fusarium oxysporum. Despite compromised JA-dependent defense responses, the JA perception mutant coronatine insensitive 1 (coi1), but not JA biosynthesis mutants, exhibited a high level of resistance to wilt disease caused by F. oxysporum. This response was independent from salicylic acid-dependent defenses, as coi1/NahG plants showed similar disease resistance to coi1 plants. Inoculation of reciprocal grafts made between coi1 and wild-type plants revealed that coi1-mediated resistance occurred primarily through the coi1 rootstock tissues. Furthermore, microscopy and quantification of fungal DNA during infection indicated that coi1-mediated resistance was not associated with reduced fungal penetration and colonization until a late stage of infection, when leaf necrosis was highly developed in wild-type plants. In contrast to wild-type leaves, coi1 leaves showed no necrosis following the application of F. oxysporum culture filtrate, and showed reduced expression of senescence-associated genes during disease development, suggesting that coi1 resistance is most likely achieved through the inhibition of F. oxysporum-incited lesion development and plant senescence. Together, our results indicate that F. oxysporum hijacks non-defensive aspects of the JA-signaling pathway to cause wilt-disease symptoms that lead to plant death in Arabidopsis.

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A critical role of two positively charged amino acids in the Jas motif of Arabidopsis JAZ proteins in mediating coronatine‐ and jasmonoyl isoleucine‐dependent interactions with the COI1 F‐box protein

Cited by 331 publications

References 31 publications

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

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

Salicylic Acid Suppresses Jasmonic Acid Signaling Downstream of SCFCOI1-JAZ by Targeting GCC Promoter Motifs via Transcription Factor ORA59

Fusarium oxysporum hijacks COI1‐mediated jasmonate signaling to promote disease development in Arabidopsis

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