Copper toxicity affects indolic glucosinolates and gene expression of key enzymes for their biosynthesis in Chinese cabbage

Tahereh A. Aghajanzadeh*, Dharmendra H. Prajapati, Meike Burow

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

    3 Citations (Scopus)


    Excessive levels of Cu2+ are phytotoxic and exposure of Chinese cabbage to elevated Cu2+ concentrations led to reduction of the plant biomass. To get more insight into the role of glucosinolates upon copper stress, the impact of elevated Cu2+ levels on glucosinolates biosynthesis were studied in Chinese cabbage. The content of total glucosinolates was only elevated in the roots, mostly due to indolic and aromatic glucosinolates. The results showed a higher contribution of indolic glucosinolates, notably glucobrassicin, a 2- and 4-fold increase in Chinese cabbage exposed to 5 and 10 µM Cu2+, respectively. Furthermore, the increase in the indolic glucosinolates was accompanied by enhanced transcript levels of CYP79B2 and CYP83B1, two genes involved in biosynthesis of indolic glucosinolates, and that of the MYB51, a transcription factor involved in regulation of indolic glucosinolate biosynthesis pathway, at elevated Cu2+ concentrations. In addition, total sulfur and nitrogen remained unaffected in the root, but total glucosinolate was significantly enhanced upon exposure to elevated Cu2+. This result may show that relatively more sulfur and nitrogen was channeled into glucosinolates in the root. In conclusion, accumulation of indolic glucosinolates in the root can be considered as a strategy for Chinese cabbage to combat elevated Cu2+ concentrations.

    Original languageEnglish
    Pages (from-to)1288–1301
    Number of pages14
    JournalArchives of agronomy and soil science
    Issue number9
    Early online date14-Sep-2019
    Publication statusPublished - 2020


    • Chinese cabbage
    • copper
    • gene expression
    • indolic glucosinolate
    • sulfur metabolism
    • AUXIN
    • IMPACT
    • CYP83B1
    • CYP79F1

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