Signal cross talk in Arabidopsis exposed to cadmium, silicon, and Botrytis cinerea

Catalina Cabot, Berta Gallego, Soledad Martos, Juan Barceló, Charlotte Poschenrieder

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46 Citations (Scopus)


The role of defence gene expression triggered by Cd toxicity in the plant's response to Botrytis cinerea was investigated in Arabidopsis thaliana Columbia 0. Silicon (0 or 1. 5 mM) and Cd (0, 1 or 10 μM) were supplied to 3-month-old solution-cultured plants. After 3 days, half of the plants of each treatment were inoculated with Botrytis. Supplied Cd concentrations were below the toxicity threshold and did not cause shoot growth inhibition or evidence of oxidative stress, while Botrytis infection severely decreased plant growth in all treatments. The expression of marker genes PR1 and BGL2 for the salicylic acid (SA) and the PDF1. 2 for the jasmonic acid-ethylene (JA-ET) signalling pathways was enhanced in 10 μM Cd-treated non-infected plants. Twenty hours after inoculation, PDF1. 2 expression showed a strong increase in all treatments, while enhanced PR1, BGL2, and CHIB expression was only found 7 days after infection. A great synergistic effect of Cd and Botrytis on PDF1. 2 expression was found in 10 μM Cd-treated plants. Silicon decreased PR1, BGL2, and CHIB, while increasing PDF1. 2 expression, which indicates its role as a modulator of the signalling pathways involved in the plant's response to fungal infection. Botrytis growth decreased in 10 μM Cd-treated plants, which could be due to the combined effects of Cd and Botrytis activating the SA and JA-ET-mediated signalling pathways. Taken together, our results provide support for the view that Cd concentrations close to the toxicity threshold induce defence signalling pathways which potentiate the plant's response against fungal infection. © 2012 Springer-Verlag Berlin Heidelberg.
Original languageEnglish
Pages (from-to)337-349
Publication statusPublished - 1 Jan 2013


  • Ethylene-dependent signalling pathways
  • Jasmonate-dependent signalling pathways
  • Salicylate-dependent signalling pathways

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