It is also very important to search for possible roles of the variable regions of SGT1 to clarify their role in HSP90 chaperone function. The cellular metabolism of most yeasts, including Saccharomyces cerevisiae, is set to run essentially on glucose. When this yeast encounters harsh conditions in niches deprived from Irisflorentin glucose, the ability to transport and metabolize non-fermentable carbon sources is crucial for its survival. In this manner, the uptake of short-chain carboxylic acids across the plasma membrane plays a defining role in the metabolism of yeast cells and in its pH-stasis. Physiological studies, carried out in this baker��s yeast, identified two distinct monocarboxylate proton symporters, strongly repressed by glucose, with different specificities and regulation. A permease involved in the uptake of lactate-pyruvateacetate and propionate was identified in lactic or pyruvic acid-S. cerevisiae grown cells, being encoded by JEN1, whereas, an acetate-proprionate-formate permease was found in ethanol or acetic acid grown cells, with no obvious gene candidate at that time. Later, ADY2 was identified as the acetate permease encoding gene in S. cerevisiae. In an early attempt to identify the genes involved in acetateproprionate-formate transport, classical genetic studies were carried out. The strain S. cerevisiae W303-1A was subjected to UV mutagenesis, in order to obtain mutants affected in the ability to utilize acetic acid, but unaffected on the capacity to grow in ethanol, as the sole carbon and energy source. According to this strategy, it was hypothesised that mutants specifically affected in monocarboxylate permease activity could be found. A mutant clone, exhibiting growth on ethanol, but with pronounced growth defect in a medium with acetic acid, as the sole carbon and energy ZINC00881524 source, was isolated. Further genotypic characterization of the Ace8 mutant led to the identification of the DHH1 gene as a most likely candidate for explaining the Ace8 phenotype. Indeed, the transformation of Ace8 cells with a genomic fragment containing DHH1 restored their capacity to grow on acetate and the deletion of DHH1 presented slower growth rates than the isogenic wild-type on acetic acid.