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Yeast genes YOL002C and SUL1 are involved in neomycin resistance

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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.

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Castro, I., Cabral, D., Trópia, M. et al. Yeast genes YOL002C and SUL1 are involved in neomycin resistance. World Journal of Microbiology and Biotechnology 17, 399–402 (2001). https://doi.org/10.1023/A:1016707627056

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  • DOI: https://doi.org/10.1023/A:1016707627056

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