Nuclear–mitochondrial cross-talk during heat shock in Arabidopsis cell culture
Article first published online: 20 SEP 2007
The Plant Journal
Volume 52, Issue 4, pages 763–778, November 2007
How to Cite
Rikhvanov, E. G., Gamburg, K. Z., Varakina, N. N., Rusaleva, T. M., Fedoseeva, I. V., Tauson, E. L., Stupnikova, I. V., Stepanov, A. V., Borovskii, G. B. and Voinikov, V. K. (2007), Nuclear–mitochondrial cross-talk during heat shock in Arabidopsis cell culture. The Plant Journal, 52: 763–778. doi: 10.1111/j.1365-313X.2007.03275.x
- Issue published online: 20 SEP 2007
- Article first published online: 20 SEP 2007
- Received 02 March 2007; revised 20 July 2007; accepted 26 July 2007.
- heat-shock proteins;
- induced thermotolerance;
- programmed cell death
Apart from energy generation, mitochondria perform a signalling function determining the life and death of a cell under stress exposure. In the present study we have explored patterns of heat-induced synthesis of Hsp101, Hsp70, Hsp17.6 (class I), Hsp17.6 (class II) and Hsp60, and the development of induced thermotolerance in Arabidopsis thaliana cell culture under conditions of mitochondrial dysfunction. It was shown that treatment by mitochondrial inhibitors and uncouplers at the time of mild heat shock downregulates HSP synthesis, which is important for induced thermotolerance in plants. The exposure to elevated temperature induced an increase in cell oxygen consumption and hyperpolarization of the inner mitochondrial membrane. Taken together, these facts suggest that mitochondrial functions are essential for heat-induced HSP synthesis and development of induced thermotolerance in A. thaliana cell culture, suggesting that mitochondrial–nuclear cross-talk is activated under stress conditions. Treatment of Arabidopsis cell culture at 50°C initiates a programmed cell death determined by the time course of viability decrease, DNA fragmentation and cytochrome c release from mitochondria. As treatment at 37°C protected Arabidopsis cells from heat-induced cell death, it may be suggested that Hsp101, Hsp70 and small heat-shock proteins, the synthesis of which is induced under these conditions, are playing an anti-apoptotic role in the plant cell. On the other hand, drastic heat shock upregulated mitochondrial Hsp60 synthesis and induced its release from mitochondria to the cytosol, indicating a pro-apoptotic role of plant Hsp60.