ArticleMolecular & general genetics : MGG1989
Rhizoxin resistant mutants with an altered beta-tubulin gene in Aspergillus nidulans.
Article in Molecular & general genetics : MGG, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- Phase II clinical trials with rhizoxin in breast cancer and melanoma. The EORTC Early Clinical Trials Group.British journal of cancer · 1996Trial
- A new tubulin-binding site and pharmacophore for microtubule-destabilizing anticancer drugs.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Regulatory volume decrease in Leishmania mexicana: effect of anti-microtubule drugs.Memorias do Instituto Oswaldo Cruz · 2013Article
- Isolation and identification of rhizoxin analogs from Pseudomonas fluorescens Pf-5 by using a genomic mining strategy.Applied and environmental microbiology · 2008Article
- Antimicrotubular drugs binding to vinca domain of tubulin.Molecular and cellular biochemistry · 2003Review
- Molecular basis for determining the sensitivity of eucaryotes to the antimitotic drug rhizoxin.Molecular & general genetics : MGG · 1990Article
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3 authors at 1 institution in 1 country.
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Abstract
Rhizoxin and ansamitocin P-3 (a maytansinoid compound), potent inhibitors of mammalian brain tubulin assembly, inhibit growth of a variety of fungi including Aspergillus nidulans. Mutants of A. nidulans, benA10 which is a benomyl resistant beta-tubulin gene mutant and tubA1 which is a benomyl supersensitive alpha-tubulin gene mutant, were both sensitive to rhizoxin and ansamitocin P-3 to the same extent as wild-type strains. We isolated 18 rhizoxin resistant mutants of A. nidulans. All of these mutants were cross-resistant to ansamitocin P-3, but not to benzimidazole antimitotic drugs. These mutants mapped to two loci, rhiA and rhiB, and all of those with high resistance mapped to rhiA. The fact that the protein extracts of rhiA mutants lost rhizoxin binding affinity and that rhiA was closely linked to benA, the major beta-tubulin gene in A. nidulans, indicated that rhiA must be a structural gene for beta-tubulin and that rhiA mutants are a new class of beta-tubulin gene mutants. All of this suggested that, in A. nidulans, these antimitotic drugs bind to beta-tubulin, and that rhizoxin and ansamitocin P-3 share the same binding site but the site does not overlap with the benzimidazole binding site. Protein extracts from a rhiB mutant retained rhizoxin binding affinity, therefore this rhizoxin resistance mechanism should not be a tubulin mediated process.
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