Two transgenic potato lines, T1 and T2, expressing the trehalose-6-phosphate synthase (TPS1) gene of yeast were isolated. In our experimental approach, we applied two novelties, namely the fusion of the drought-inducible promoter StDS2 to TPS1 and a marker-free transformation method. In contrast to the expected drought-induced expression, only a very low constitutive TPS1 expression was detected in the transgenic lines, probably due to chromosomal position effects. The observed expression pattern, however, was sufficient to alter the drought response of plants. Detached leaves of T1 and T2 showed an 8 h delay in wilting compared to the non-transformed control. Potted plants of T1 and T2 kept water 6 days longer than control plants and maintained high stomatal conductance and a satisfactory rate of net photosynthesis. During drought treatment, CO2 assimilation rate measured at saturating CO2 level was maintained at maximum level for 6-9 days in transgenic plants while it decreased rapidly after 3 days in the wild type plants. Under optimal growth conditions, lower CO2 fixation was detected in the transgenic than in the control plants. Stomatal densities of T1 and T2 leaves were reduced by 30-40%. This may have contributed to the lower CO2 fixation rate and altered drought response.

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The results indicate that local H₂O₂ production promotes, while quenching of H₂O₂ impairs disulfide formation. The contribution of H₂O₂ to disulfide bond formation previously observed in vitro can be also shown in cellular and in vivo systems.

Augmenter of liver regeneration (ALR) contributes to mitochondrial biogenesis, maintenance and to the physiological operation of mitochondria. The depletion of ALR has been widely studied and had serious consequences on the mitochondrial functions. However the inverse direction, the effect of the depletion of mitochondrial electron transfer chain and mtDNA on ALR expression has not been investigated yet. Thus mtDNA depleted, ρ(0) cell line was prepared to investigate the role of mitochondrial electron transfer chain and mtDNA on ALR expression. The depletion of mtDNA has not caused any difference at mRNA level, but at protein level the expression of ALR has been markedly increased. The regulatory role of ATP and ROS levels could be ruled out because the treatment of the parental cell line with different respiratory inhibitors and uncoupling agent could not provoke any changes in the protein level of ALR. The effect of mtDNA depletion on the protein level of ALR has been proved not to be liver specific, since the phenomenon could be observed in the case of two other, non-hepatic cell lines. It seems the level of mtDNA and/or its products may have regulatory role on the protein level of ALR. The up-regulation of ALR can be a part of the adaptive response in ρ(0) cells that preserves the structural integrity and the transmembrane potential despite the absence of protein components encoded by the mtDNA.

Each eukaryotic cell of multicellular organisms must be able to maintain its integrity by sensing both external and internal stimuli. The primary goal of the generated response mechanism is to drive back the system to the former or to a new homeostatic state. Moreover, the response has to provide an accurate survival-or-death decision to avoid any "misunderstanding" and its unwanted consequences. New data revealed that a systems-level crosstalk of molecular networks has an essential role in achieving the correct characteristic of the response. Although many molecular components of these processes already have been revealed, several elements and regulatory connections of crosstalk are still missing. These "gaps" of the complex control networks make hardly impossible to present comprehensive models. Therefore we approach the questions from a systems biology aspect by combining the experimental results with the special technique of mathematical modelling. In this short report we discuss some novel and preliminary data gained by this approach on the crosstalk between life and death decisions under cellular stress, to get a systems biological view of these networks.