Ontology highlight
ABSTRACT:
RESULTS: Metabolomic analyses identified signatory biomarkers involved in the establishment of a pre-conditioned state following Aza and Hxa treatment. Both inducers affected the metabolomes in a similar manner and generated common biomarkers: caffeoylputrescine glycoside, cis-5-caffeoylquinic acid, feruloylglycoside, feruloyl-3-methoxytyramine glycoside and feruloyl-3-methoxytyramine conjugate. Subsequently, quantitative real time-PCR was used to investigate the expression of inducible defense response genes: phenylalanine ammonia lyase, hydroxycinnamoyl CoA quinate transferase and hydroxycinnamoyl transferase to monitor activation of the early phenylpropanoid pathway and chlorogenic acids metabolism, while ethylene response element-binding protein, small sar1 GTPase, heat shock protein 90, RAR1, SGT1, non-expressor of PR genes 1 and thioredoxin were analyzed to report on signal transduction events. Pathogenesis-related protein 1a and defensin were quantified to investigate the activation of defenses regulated by salicylic acid and jasmonic acid respectively. The qPCR results revealed differential expression kinetics and, in general (except for NPR1, Thionin and PR1a), the relative gene expression ratios observed in the Hxa-treated cells were significantly greater than the expression observed in the cells treated with Aza.
CONCLUSIONS: The results indicate that Aza and Hxa have a similar priming effect through activation of genes involved in the establishment of systemic acquired resistance, associated with enhanced synthesis of hydroxycinnamic acids and related conjugates.
INSTRUMENT(S): SYNAPT HDMS (Waters)
PROVIDER: MTBLS559 | MetaboLights | 2018-10-17
REPOSITORIES: MetaboLights
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| Pooled_sampleA_1a.raw.zip | Raw | |||
| Pooled_sampleA_1b.raw.zip | Raw | |||
| Pooled_sampleA_2a.raw.zip | Raw | |||
| Pooled_sampleA_2b.raw.zip | Raw | |||
| Pooled_sampleA_3a.raw.zip | Raw |
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