Abstract
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 proteasome-mediated 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 β-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.
Highlights
Within their natural habitats, plants intimately interact simultaneously or sequentially with a broad range of microbial pathogens and insect herbivores with different lifestyles and invasion strategies
We checked whether overexpression of JAZ10 without a functional Jas domain would lead to suppression of the jasmonic acid (JA) pathway in our experimental setup
5-week-old plants of wild-type Columbia-0 (Col-0) and 35S: JAZ10D #OE4A and 35S:JAZ10D #OE4B, which overexpress a truncated form of JAZ10 that lacks part of the Jas domain (Yan et al, 2007), were treated with methyl jasmonate (MeJA)
Summary
Plants intimately interact simultaneously or sequentially with a broad range of microbial pathogens and insect herbivores with different lifestyles and invasion strategies. In Arabidopsis thaliana, transcriptome analyses of wild-type and mutant plants challenged with different attackers revealed complex antagonistic and synergistic regulatory relationships between SA and JA signaling sectors of the plant immune signaling network (Glazebrook et al, 2003; De Vos et al, 2005; Sato et al, 2010) Such hormonal crosstalk is thought to optimize the immune response against single attackers that stimulate both the SA and the JA pathway or to prioritize one pathway over the other when plants are simultaneously or sequentially attacked by different enemies (Pieterse et al, 2012; Thaler et al, 2012). Successful pathogens and insect herbivores have been demonstrated to hijack hormone signal integration, either through the production of plant hormones, hormone mimics, or effectors that target hormone signaling components to manipulate the plant immune signaling network for their own benefit (Walling, 2008; Grant and Jones, 2009; Pieterse et al, 2012)
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