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  • 1990-1994  (3)
  • Life and Medical Sciences  (2)
  • Anthracnose Maize  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Generation-means analysis and quantitative trait locus mapping of anthracnose stalk rot genes in maize (1994)
    Springer
    Theoretical and applied genetics 89 (1994), S. 413-418 
    Details
    ISSN: 1432-2242
    Keywords: Restriction fragment length polymorphism Linkage mapping ; Multiple regression ; Anthracnose Maize
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract A generation-means analysis was performed on two maize populations, each segregating for genes conferring resistance to anthracnose stalk rot (ASR). The populations were derived from a cross of DE811ASR x DE811 and of DE811ASR x LH132. The resistant parent, DE811ASR, was obtained through introgression with MP305 as the donor and DE811 as the recurrent parent. The analysis revealed significant additive effects in both populations and a significant additive x dominant effect in the DES11ASR x DES11 population. Quantitative trait locus (QTL) mapping, using restriction fragment length polymorphism (RFLP)-based molecular markers, indicated a significant QTL on linkage group 4 in both populations. The QTL analysis confirmed additive inheritance in both populations. This work demonstrates a close correspondence between generation-means analysis and discrete observations using molecular markers. Linkage of a genetic marker to genes conferring resistance to ASR will be useful for the introgression of resistance into elite germplasm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00225375
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  • 2
    Electronic Resource
    Electronic Resource
    Identification of an amino acid substitution in the benA, β-tubulin gene of Aspergillus nidulans that confers thiabendazole resistance and benomyl supersensitivity (1990)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 17 (1990), S. 87-94 
    Details
    ISSN: 0886-1544
    Keywords: benzimidazole ; anti-microtubule agents ; carbendazim ; nocodazole ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We are using molecular genetic techniques to identify sites of interaction β-tubulin with benzimidizole anti-microtubule agents. We have developed a marker-rescue technique for cloning mutant alleles of the benA, β-tubulin gene of Aspergillus nidulans and have used the technique to clone two mutant benA alleles, benA16 and benA19. These are the only A. nidulans alleles known to confer resistance to the benzimidazole antimicrotubule agent thiabendazole and supersensitivity to other benzimidazole antimicrotubule agents including benomyl and its active breakdown product, carbendazim. benA16 has been shown, moreover, to reduce thiabendazole binding to β-tubulin. We have sequenced the two mutant alleles and have found that they carry different nucleotide changes that cause the same single amino acid substitution, valine for alanine at amino acid 165. Since thiabendazole and carbendazim differ at only one side chain, the R2 group, we conclude that the region around amino acid 165 is involved in the binding of the R2 group of benzimidazole antimicrotubule agents to β-tubulin.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970170204
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  • 3
    Electronic Resource
    Electronic Resource
    Amino acid alterations in the benA (β-tubulin) gene of Aspergillus nidulans that confer benomyl resistance (1992)
    New York, NY : Wiley-Blackwell
    Cell Motility and the Cytoskeleton 22 (1992), S. 170-174 
    Details
    ISSN: 0886-1544
    Keywords: nocodazole ; carbendazim ; antimicrotubule agents ; thiabendazole ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: We report the cloning and sequencing of 18 mutant alleles of the benA, β-tubulin gene of Aspergillus nidulans that confer resistance to the benzimidazole antifungal, antimicrotubule compounds benomyl, carbendazim, nocodazole, and thia-bendazole. In 12 cases, amino acid 6 was changed from histidine to tyrosine or leucine. In four cases, amino acid 198 was changed from glutamic acid to aspartic acid, glutamine, or lysine. In two cases, amino acid 200 was altered from phenylalanine to tyrosine. These data, along with previous data indicating that amino acid 165 is involved in the binding of the R2 group of these compounds [Jung and Oakley, 1990: Cell Motil. Cytoskeleton 17:87-94], suggest that regions of β-tubulin containing amino acids 6, 165, and 198-200 interact to form the binding site of benzimidazole antimicrotubule agents. These results also suggest that the presence of phenylalanine at amino acid 200 contributes to the great sensitivity of many fungi to benzimidazole antimicrotubule agents. © 1992 Wiley-Liss, Inc.
    Additional Material: 1 Tab.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cm.970220304
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