Low oleic acid-derived repression of jasmonic acid-inducible defense responses requires the WRKY50 and WRKY51 proteins

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.     

Ozone-induced ethylene production is dependent on salicylic acid,and both salicylic acid and ethylene act in concert to regulate ozone-induced cell death

Ethylene is known to influence plant defense responses including cell death in response to both biotic and abiotic stress factors. However, whether ethylene acts alone or in conjunction with other signaling pathways is not clearly understood. Ethylene overproducer mutants, eto1 and eto3, produced high levels of ethylene and developed necrotic lesions in response to an acute O3 exposure that does not induce lesions in O3-tolerant wild-type Col-0 plants. Treatment of plants with ethylene inhibitors completely blocked O3-induced ethylene production and partially attenuated O3-induced cell death. Analyses of the responses of molecular markers of specific signaling pathways indicated a relationship between salicylic acid (SA)- and ethylene-signaling pathways and O3 sensitivity. Both eto1 and eto3 plants constitutively accumulated threefold higher levels of total SA and exhibited a rapid increase in free SA and ethylene levels prior to lesion formation in response to O3 exposure. SA pre-treatments increased O3 sensitivity of Col-0, suggesting that constitutive high SA levels prime leaf tissue to exhibit increased magnitude of O3-induced cell death. NahG and npr1 plants compromised in SA signaling failed to produce ethylene in response to O3 and other stress factors suggesting that SA is required for stress-induced ethylene production. Furthermore, NahG expression in the dominant eto3 mutant attenuated ethylene-dependent PR4 expression and rescued the O3-induced HR (hypersensitive response) cell death phenotype exhibited by eto3 plants. Our results suggest that both SA and ethylene act in concert to influence cell death in O3-sensitive genotypes, and that O3-induced ethylene production is dependent on SA.