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Transcriptome responses to the natural phytotoxin t‐chalcone in Arabidopsis thaliana L.

Díaz‐Tielas, Carla, Graña, Elisa, Sánchez‐Moreiras, Adela M, Reigosa, Manuel J, Vaughn, Justin N, Pan, Zhiqiang, Bajsa‐Hirschel, Joanna, Duke, Mary V, Duke, Stephen O
Pest management science 2019 v.75 no.9 pp. 2490-2504
4-hydroxyphenylpyruvate dioxygenase, Arabidopsis thaliana, Lemna aequinoctialis, abscisic acid, auxins, biosynthesis, bleaching, enzyme inhibition, flavonoids, genes, heat shock proteins, herbicides, mechanism of action, oxidative stress, phytotoxins, roots, seedlings, sequence analysis, shoots, taxonomy, transcription factors, transcriptome, tyrosine, xenobiotics
BACKGROUND: New modes of action are needed for herbicides. The flavonoid synthesis intermediate t‐chalcone causes apoptosis‐like symptoms in roots and bleaching of shoots of Arabidospsis, suggesting a unique mode of action as a phytotoxin. RESULTS: Using RNA‐Seq, transcriptome changes were monitored in Arabidopsis seedlings during the first 24 h of exposure (at 1, 3, 6, 12 and 24 h) to 21 μm t‐chalcone (I₅₀ dose), examining effects on roots and shoots separately. Expression of 892 and 1000 genes was affected in roots and shoots, respectively. According to biological classification, many of the affected genes were transcription factors and genes associated with oxidative stress, heat shock proteins, xenobiotic detoxification, ABA and auxin biosynthesis, and primary metabolic processess. These are secondary effects found with most phytotoxins. Potent phytotoxins usually act by inhibiting enzymes of primary metabolism. KEGG pathway analysis of transcriptome results from the first 3 h of t‐chalcone exposure indicated several potential primary metabolism target sites for t‐chalcone. Of these, p‐hydroxyphenylpyruvate dioxygenase (HPPD) and tyrosine amino transferase were consistent with the bleaching effect of the phytotoxin. Supplementation studies with Lemna paucicostata and Arabidiopsis supported HPPD as the target, although in vitro enzyme inhibition was not found. CONCLUSIONS: t‐Chalcone is possibly a protoxin that is converted to a HPPD inhibitor in vivo. © 2019 Society of Chemical Industry