SummaryApart 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 mitochondrialnuclear 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.

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Abstract. Auxins (IAA, NAA, p-CPA) caused 20-30% promotion of respiration of auxin-dependent cell cultures of Nicotiana tabacum, Glycine max, Taraxacum mongolica, and Atriplex sp. and had small if any effect on respiration of auxin-independent cell cultures of Rubus sp. and Scorzonera hispanica. Antiauxin (p-CPIBA) did not affect the respiration. The auxin effect on the respiration of tobacco cells was revealed 10 min after its addition to the suspension and reached a maximum value in 60 rain. This stimulation preceded the induction of cell division by auxin. Mitochondria isolated from auxin-treated tobacco cells had greater oxidative and phosphorylative activity than mitochondria from untreated cells. However, isolated mitochondria did not respond to auxin. The inhibitors of respiration (cyanide, monoiodoacetate, malonate, and 2,4-dinitrophenol) eliminated auxin effect on the respiration and cell division. It is concluded that the promotion of respiration is a common event for the auxin effects both on cell extension and on cell division. This promotion is necessary for the induction of cell division and is exerted via direct activation of mitochondria in situ.Auxins not only stimulate cell extension but also induce cell division, especially in isolated culture. The stimulation of cell extension is usually accompanied by the promotion of respiration (Audus 1960, Bonner andBandurski 1952). However, it is uncertain if respiration is promoted when auxins induce cell division.Normal (nontumorous) plant cells cultured in suspension are the most suitable objects to elucidate this problem, because their division has an obligatory dependence on exogenous auxin. Many authors have reported that initiation and growth of callus and cell cultures in the media with auxins was accom-

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