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Site-directed mutagenesis of Saccharomyces cerevisiae β-tubulin: interaction between residue 167 and benzimidazole compounds
Journal article   Open access   Peer reviewed

Site-directed mutagenesis of Saccharomyces cerevisiae β-tubulin: interaction between residue 167 and benzimidazole compounds

Jing Li, Santosh K Katiyar and Thomas D Edlind
FEBS letters, v 385(1), pp 7-10
1996
PMID: 8641470
url
https://doi.org/10.1016/0014-5793(96)00334-1View
Published, Version of Record (VoR) Open

Abstract

Microtubule Saccharomyces cerevisiae Benzimidazole β-Tubulin
Benzimidazoles are widely used as anthelmintic agents and systemic fungicides. In susceptible organisms, benzimidazoles bind to β-tubulin and block microtubule polymerization. To further characterize this interaction, site-directed mutagenesis followed by gene replacement was used to change Saccharomyces cerevisiae β-tubulin residue Phe-167 to Tyr. Consistent with previous studies, this mutation resulted in at least 3–4-fold decreased sensitivity to the benzimidazole derivatives carbendazim and nocodazole. The Tyr-167 mutant was cold sensitive, implying a direct effect on benzimidazole binding rather than a nonspecific increase in microtubule stability. Surprisingly, the mutant had 8-fold increased sensitivity to the derivative benomyl, which is structurally identical to carbendazim except at position 1. This suggests that residue 167 interacts with benzimidazoles in the vicinity of the 1-position.

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Web of Science research areas
Biochemistry & Molecular Biology
Biophysics
Cell Biology
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