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|Title:||Yeast genes YOL002C and Sul1 are involved in neomycine resistance.|
|Authors:||Castro, Ieso de Miranda|
Cabral, D. B.
Trópia, Maria José Magalhães
Barnabé, Fabiana Maria de Almeida
Brandão, Rogélio Lopes
|Citation:||CASTRO, 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.|
|Abstract:||In 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.|
|Appears in Collections:||DEFAR - Artigos publicados em periódicos|
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