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  • 1
    ISSN: 1432-0983
    Keywords: Diethofencarb ; Benzimidazole resistance ; β-tubulin ; Neurospora crassa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: 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 β-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 β-tubulin gene. The amino acid changes in β-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 β-tubulin in these mutants was Gly, which is the same as in strain F914. β-tubulin genes with 198Glu were constructed by site-directed mutagenesis. The altered β-tubulin genes derived from FR511 and FR421 transformed the wild-type strain to resistance to MBC, indicating that 250Phe and 237Ala in β-tubulin are responsible for resistance not only to diethofencarb but also to MBC.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 145 (1990), S. 428-433 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Transformed Fisher rat fibroblast cell lines by Abelson murine leukemia virus frequently revert to the normal phenotype in usual culture conditions. Molecular Biological analysis of thre revertant clones isolated from the transformants showed that their morphological reversions were due to inactivation of the v-abl oncogene at multiple steps including transcription, translation or v-abl protein kinase activity itself without any change in structural gene expression of helper virus. These findings suggest the existence of a specific mechanism(s) for elimination of the v-abl oncogene by segregation, mutation, or gene rearrangement in these cells.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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