Castro, Ieso de MirandaCabral, Daniela BastosTrópia, Maria José MagalhãesBarnabé, Fabiana Maria de AlmeidaBrandão, Rogélio Lopes2017-03-202017-03-202001CASTRO, I. de M. et al. Yeast genes YOL002C and Sul1 are involved in neomycine resistance. World Journal Of Microbiology And Biotechnology, v. 17, n. 4, p.399-402, 2001. Disponível em: <http://link.springer.com/article/10.1023/A:1016707627056>. Acesso em: 10 jan. 2017.1573-0972http://www.repositorio.ufop.br/handle/123456789/7393In previous studies we suggested the importance of the control of plasma membrane H+-ATPase by a phosphatidylinositol-like pathway for cellular proton extrusion in Saccharomyces cerevisiae (Brandão et al. 1994; Coccetti et al. 1998). The observations that provided the model above include the inhibition of the glucose-induced activation of the plasma membrane H+-ATPase as well as the inhibition of the glucose-induced external acidification by neomycin, a known inhibitor of the phosphatidylinositol turnover in eukaryotic cells. In this work, using two libraries, we isolated two yeast clones that were able to prevent the inhibition of glucose-induced activation of the H+-ATPase by neomycin. We show that the YOL002C gene, which encodes a protein of unknown function, and the SUL1 gene, which is a sulphate transporter belonging to the major facilitator superfamily, suppress growth inhibition by neomycin. However, they are not required for glucose-induced activation of the plasma membrane H+-ATPase. The resistance of the clones to neomycin is probably related to the level and/or activity of proteins functioning as drug extrusion pumps.en-USrestritoGrowth inhibitionArtigo publicado em periodicohttp://link.springer.com/article/10.1023/A:1016707627056https://doi.org/10.1023/A:1016707627056