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Yeast genes YOL002C and SUL1 are involved in neomycin resistance

In previous studies we suggested the importance of the control of plasma membrane H^sup +^-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 i...

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Bibliographic Details
Published in:World journal of microbiology & biotechnology 2001-06, Vol.17 (4), p.399-402
Main Authors: CASTRO, I. M, CABRAL, D. B, TROPIA, M. J. M, ALMEIDA, F. M, BRANDAO, R. L
Format: Article
Language:English
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Summary:In previous studies we suggested the importance of the control of plasma membrane H^sup +^-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^sup +^-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^sup +^-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^sup +^-ATPase. The resistance of the clones to neomycin is probably related to the level and/or activity of proteins functioning as drug extrusion pumps.[PUBLICATION ABSTRACT]
ISSN:0959-3993
1573-0972
DOI:10.1023/A:1016707627056