An early Ca[sup]2+ influx is a prerequisite to thaxtomin A-induced cell death in Arabidopsis thaliana cells

• Published in: Journal of experimental botany Vol. 59; no. 15; p. 4259
• Main Authors: Errakhi, R, Dauphin, A, Meimoun, P, Lehner, A, Reboutier, D, Vatsa, P, Briand, J, Madiona, K, Rona, J P, Barakate, M, Wendehenne, D, Beaulieu, C, Bouteau, F
• Format: Journal Article
• Language: English
• Published: Oxford Oxford Publishing Limited (England) 01-11-2008
• ISSN: 0022-0957; 1460-2431
• DOI: 10.1093/jxb/ern267

The pathogenicity of various Streptomyces scabies isolates involved in potato scab disease was correlated with the production of thaxtomin A. Since calcium is known as an essential second messenger associated with pathogen-induced plant responses and cell death, it was investigated whether thaxtomin A could induce a Ca[sup]2+ influx related to cell death and to other putative plant responses using Arabidopsis thaliana suspension cells, which is a convenient model to study plant-microbe interactions. A. thaliana cells were treated with micromolar concentrations of thaxtomin A. Cell death was quantified and ion flux variations were analysed from electrophysiological measurements with the apoaequorin Ca[sup]2+ reporter protein and by external pH measurement. Involvement of anion and calcium channels in signal transduction leading to programmed cell death was determined by using specific inhibitors. These data suggest that this toxin induces a rapid Ca[sup]2+ influx and cell death in A. thaliana cell suspensions. Moreover, these data provide strong evidence that the Ca[sup]2+ influx induced by thaxtomin A is necessary to achieve this cell death and is a prerequisite to early thaxtomin A-induced responses: anion current increase, alkalization of the external medium, and the expression of PAL1 coding for a key enzyme of the phenylpropanoid pathway.