Bakerīs yeast (Saccharomyces cerevisiae) is exposed to different adverse growth conditions, such as osmotic or oxidative stress, both in nature and in industrial processes. Osmotic stress triggers a complex response in eukaryotic cells in order to survive, repair damage and adjust the cells to the new environmental conditions. This adaptation affects multiple physiological functions and entails the induction of defense gene expression through the activation of signaling transduction pathways. MAP kinase cascades are among the most important pathways to respond to stress, and they are evolutionarily conserved in all higher eukaryotes. Specifically, the HOG (High Osmolarity Glycerol) pathway responds to hyperosmotic stress and is conserved in yeast, plants and mammals. Its Hog1p MAP kinase is quickly activated upon stress and coordinates an adaptive response at several physiological levels such as the modulation of ion transport activity at the plasma membrane, the transition through the cell cycle, mRNA translation and transcriptional activation of hundreds of genes in the nucleus. 
  The transcriptional program upon osmotic stress is surprisingly complex in yeast and involves several partially redundant transcription factors. Therefore, the quantification of the direct binding of these factors to chromatin is the best experimental procedure to understand the genomic organization of the transcriptional program during osmotic stress. The technology of chromatin immunoprecipitation combined with microarrays (ChIP-Chip) has already been successfully applied to several transcription factors and proteins that are recruited to chromatin. 
  Previously, ChIP-Chip analyses were carried out for Sko1p, a transcription factor under control of the HOG pathway. This analysis identified the promoters of genes encoding several other regulators, such as Mot3p and Rox1p, as Sko1p targets.
  In this work a detailed study of the function of Mot3p and Rox1p during cellular stress adaptation has been carried out. The obtained results suggest that both transcriptional repressors regulate the expression of ergosterol biosynthesis genes upon osmotic stress in a  process which is controlled by the Hog1p MAP kinase. Furthermore, another control level has been identified here, which consists in the transcriptional down regulation of ECM22 encoding the main ERG gene activator, through Mot3p, Rox1p and Hog1p. Repression of ergosterol biosynthesis also occurs in oxidative stress conditions, although in this case the response is only partially dependent of Mot3p/Rox1p and Hog1p. Finally, it has been shown that the upc2-1 mutation confers severe sensitivity to salt and oxidative stress due to the hyper accumulation of ergosterol and overexpression of ERG2 and ERG11. These results highlight the relevance of the modulation of ergosterol levels to stress adaptation in yeast cells. 
  On the other hand, this thesis reveals interesting data about the complex transcriptional regulation network that operates upon osmotic stress in yeast. ChIP-Chip and ChIP-Seq technology contribute new information about the genome-wide location of the transcription factors Hot1p and Smp1p, direct targets of the Hog1p MAP kinase, and the Mot3p regulator. Detailed studies of Hot1p prove its binding to genes involved in glycerol transport and biosynthesis, and a new consensus site has been proposed for Hot1 binding to the limited set of genomic targets. Mot3p binds both osmo-inducible and -repressible promoters, adding complexity to its function in stress adaptation. Finally, in the case of Smp1p, an unexpected binding within the coding sequences of osmoinducible genes has been shown, suggesting a function of Smp1p beyond transcriptional initiation.