Low Oleic Acid-Derived Repression of Jasmonic Acid-Inducible Defense Responses Requires the WRKY50 and WRKY51 Proteins    

Abstract

Signaling induced upon a reduction in oleic acid (18:1) levels simultaneously up-regulates salicylic acid (SA)-mediated responses and inhibits jasmonic acid (JA)-inducible defenses, resulting in enhanced resistance to biotrophs but increased susceptibility to necrotrophs. SA and the signaling component Enhanced Disease Susceptibility1 function redundantly in this low-18:1-derived pathway to induce SA signaling but do not function in the repression of JA responses. We show that repression of JA-mediated signaling under low-18:1 conditions is mediated via the WRKY50 and WRKY51 proteins. Knockout mutations in WRKY50 and WRKY51 lowered SA levels but did not restore pathogenesis-related gene expression or pathogen resistance to basal levels in the low-18:1-containing Arabidopsis (Arabidopsis thaliana) mutant, suppressor of SA insensitivity2 (ssi2). In contrast, both JA-inducible PDF1.2 (defensin) expression and basal resistance to Botrytis cinerea were restored. Simultaneous mutations in both WRKY genes (ssi2 wrky50 wrky51) did not further enhance the JA or Botrytis-related responses. The ssi2 wrky50 and ssi2 wrky51 plants contained high levels of reactive oxygen species and exhibited enhanced cell death, the same as ssi2 plants. This suggested that high reactive oxygen species levels or increased cell death were not responsible for the enhanced susceptibility of ssi2 plants to B. cinerea. Exogenous SA inhibited JA-inducible PDF1.2 expression in the wild type but not in wrky50 or wrky51 mutant plants. These results show that the WRKY50 and WRKY51 proteins mediate both SA-and low-18:1-dependent repression of JA signaling.

Arabidopsis MYC Transcription Factors Are the Target of Hormonal Salicylic Acid/Jasmonic Acid Cross Talk in Response to Pieris brassicae Egg Extract

“…Multiple TGA transcription factor mutants tga235 and tga2356 are blocked in SA-mediated inhibition of JA (Zander et al, 2010;Leon-Reyes et al, 2010b). For WRKY transcription factors, wrky50 and wrky51 mutants do not show SA suppression of JA-mediated PDF1.2 expression (Gao et al, 2011).…”

Tobacco mosaic virus-directed reprogramming of auxin/indole acetic acid protein transcriptional responses enhances virus phloem loading

“…Interestingly, the five upregulated WRKYs have all been shown previously to be induced in response to SA treatment, whereas the four that were down-regulated were all undetectable (WRKY12, -14, and -35) or repressed (WRKY44) by SA treatment (69). WRKY38 expression has been linked to the degradation of NPR1 and in combination with WRKY62 is required for systemic acquired resistance (70), and WRKY51 has been shown to mediate SA-dependent repression of JA signaling (71). Another important regulator affecting the antagonism between SA-and JA-mediated signaling is GRX480, which showed a sixfold increase in IAA26-P108H-GFP plants (72).…”

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

“…Expression of a large part of the WKRY transcription factors is SA responsive (Dong et al, 2003), and certain WRKYs have been described as important components in transcriptional regulation of SA-responsive gene expression (Wang et al, 2006;van Verk et al, 2011). A recent report showed that SA-mediated suppression of JA-induced PDF1.2 gene expression was abolished in wrky50 single and wrky50 wrky51 double knockout mutants, indicating that these WRKYs play an important role in SA/JA crosstalk (Gao et al, 2011). Although we did find an overrepresentation of the WRKY binding site (W-box) in promoters of SA/JA crosstalk genes (Figure 4), the PDF1.2 promoter does not contain a W-box element.…”

“…Several other molecular players in SA/ JA crosstalk have been identified, including the mitogen-activated protein kinase MPK4 (Petersen et al, 2000), the lipase-like proteins ENHANCED DISEASE SUSCEPTIBILITY1 and PHY-TOALEXIN-DEFICIENT4 (Brodersen et al, 2006), the fatty acid desaturase SUPPRESSOR OF SA INSENSITIVITY2 (Kachroo et al, 2003), glutaredoxin GRX480 (Ndamukong et al, 2007;Zander et al, 2010), and class II TGA and WRKY transcription factors (Li et al, 2004;Mao et al, 2007;Ndamukong et al, 2007;Leon-Reyes et al, 2010a;Zander et al, 2010;Gao et al, 2011). Mutation or ectopic expression of the corresponding genes often have contrasting effects on SA and JA signaling and on resistance against biotrophs and necrotrophs, indicating that these proteins are important regulators of SA/JA crosstalk.…”