Mild heat shock induces the synthesis of heat shock proteins (HSP) protecting the cell from damages during subsequent severe heat shock. The nature of the signal inducing transcription of Hsp genes is poorly investigated. We studied the effects of mitochondrial inhibitors, sodium azide and dinitrophenol (DNP) on the development of induced thermotolerance and induction of Hsp101 and Hsp60 syntheses in the suspension culture of Arabidopsis thaliana. The presence of sodium azide and DNP during mild heat shock was shown to suppress heat-induced synthesis of Hsp101 and development of induced thermotolerance in the A. thaliana cultured cells. Severe heat shock (50°C) resulted in programmed cell death as was evident from reduced cell viability and cytochrome c release. The results obtained permit a supposition that the functional state of mitochondria determines Hsp gene expression in A. thaliana subjected to heat shock.