ArticleCurrent genetics1994
Amino-acid alterations in the beta-tubulin gene of Neurospora crassa that confer resistance to carbendazim and diethofencarb.
Article in Current genetics, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 34 citations in OpenAlex.
- Chlamydomonas reinhardtii tubulin-gene disruptants for efficient isolation of strains bearing tubulin mutations.PloS one · 2020Article
- Article
- Predicting Resistance by Mutagenesis: Lessons from 45 Years of MBC Resistance.Frontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously shown that increased sensitivity to diethofencarb in the carbendazim(MBC)-resistant F914 strain of Neurospora crassa is caused by a single amino-acid change in beta-tubulin, 198Glu to Gly. Three diethofencarb-resistant mutants that are also resistant to MBC were isolated from strain F914. They contained single base-pair-substitution mutations in the beta-tubulin gene. The amino acid changes in beta-tubulin, Phe from 250Leu, Val from 165Ala, and Ala from 237Thr, were responsible for diethofencarb-resistance in the mutant strains FR511, FR513, and FR421, respectively. The amino acid at position 198 of beta-tubulin in these mutants was Gly, which is the same as in strain F914. beta-tubulin genes with 198Glu were constructed by site-directed mutagenesis. The altered beta-tubulin genes derived from FR511 and FR421 transformed the wild-type strain to resistance to MBC, indicating that 250Phe and 237Ala in beta-tubulin are responsible for resistance not only to diethofencarb but also to MBC.
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