Despite being extensively studied in various organisms due to scientific, industrial and medical interest, the galactose assimilation function and regulation, and especially its interaction with other parts of cellular physiology, have not been fully elucidated yet. The post-genomic era holistic techniques ("omics") could assist towards this goal. In this paper, we holistically analyzed full-genome Saccharomyces cerevisiae transcriptional profiling data concerning its glucose- and galactose-grown wild-type (WT) physiology and its glucose-grown gal7-deficient (GAL7Delta) physiology, as these were obtained in the experiment described in Lai and Elsas (Biochem. Biophys. Res. Commun. 2000, 271, 392-400). The gal7 gene encodes for the second enzyme of the galactose assimilation, Leloir, pathway, and its deficiency in humans causes a potentially lethal disease, named "classic galactosemia". Analysis of the galactose-grown compared to the glucose-grown WT physiology indicated a significant increase in the transcriptional expression of the ribosomal machinery and decrease in the transcriptional activity of the fatty acids' beta-oxidation at the peroxisomes. Comparison of GAL7Delta to WT physiology in glucose indicated a significant transcriptional increase in the mitochondrial activity and the rate of catabolism of disaccharides, including sucrose, mannose and trehalose, towards amplified biosynthesis of the main cell wall components. Comparison with other physiological conditions indicated strong correlation between the glucose-grown GAL7Delta transcriptional physiology and the WT growth under glucose derepression conditions. Finally, the acquired results and the large number of still unknown genes that were related to the galactose assimilation regulation indicated the need for further, specifically designed, perturbations and integrated analyses of multiple levels of cellular function.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Reference||Annotation Extension|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|