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  • 1
    Electronic Resource
    Electronic Resource
    Chromosome location of genes for resistance to powdery mildew in common wheat (Triticum aestivum L.) 1. Mlk and other alleles at the Pm3 locus (1993)
    Springer
    Euphytica 68 (1993), S. 223-229 
    Details
    ISSN: 1573-5060
    Keywords: common wheat ; Triticum aestivum ; resistance genes ; Erysiphe graminis tritici ; powdery mildew ; monosomic analysis ; allelism tests
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: Summary Several wheat cultivars/lines were inoculated with isolates of Erysiphe graminis tritici to identify new genes/alleles for resistance. The wheats were tested with 13 isolates that had been characterized from responses on differential lines with known resistance genes. Gene Mlk which occurs in cultivars ‘Kolibri’, ‘Syros’, ‘Ralle’ and several other European common wheats was found to be an allele at the Pm3 locus and is now designated Pm3d. The mildew resistance in an old Australian wheat, ‘W150’, is conferred by a single gene also allelic to Pm3 and now designated Pm3e. The near-isogenic line ‘Michigan Amber/8*Cc’ possesses another allele now designated Pm3f. A Syrian land variety of common wheat shows mildew resistance that is conditioned by the combination of genes Pm1 and Pm3a. Finally, two accessions of Triticum aestivum ssp. sphaerococcum appeared to possess the Pm3c allele.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00029876
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  • 2
    Electronic Resource
    Electronic Resource
    Genetic analysis of aflatoxin B1 activation in rat hepatoma cells (1990)
    Springer
    Molecular genetics and genomics 222 (1990), S. 291-296 
    Details
    ISSN: 1617-4623
    Keywords: Aflatoxin B1 ; Cytochrome P450 ; Rat hepatoma cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary We present a strategy to elucidate the rate-limiting steps in activation of carcinogenic compounds by cytochromes P450. The principle was to select Reuber rat hepatoma cells for resistance to a procarcinogen. The hypothesis was that resistant cells should be systematically deficient in the P450 enzyme(s) involved in the activation process. Here we present an example of the use of this approach using aflatoxin B1 (AFB1), a potent hepatocarcinogen, as the selective agent. Parental cells as well as individual and pooled colonies selected for AFB1 resistance from three independent rat hepatoma lines were characterized for their content of 1) mRNA hybridizing to cDNA and/or oligonucleotide probes for cytochromes P450IIB1, P450IIB2 and albumin; and 2) aldrin epoxidase activity. Parental aflatoxin B1-sensitive cells were shown to express P450IIB1 but not P450IIB2. The majority of the aflatoxin B1-resistant clones failed to accumulate cytochrome P450IIB1 mRNA and expressed no or only very low aldrin epoxidase activity. Albumin mRNA levels remained unchanged, demonstrating that loss of expression of cytochrome P450IIB1 was not a consequence of a general dedifferentiation event. A revertant population showing restoration of both cytochrome P450IIB1 mRNA accumulation and aldrin epoxidase activity was fully sensitive to aflatoxin B1. The correlation between expression of cytochrome P450IIB1 and sensitivity to aflatoxin B1 in both parental cells and revertants strongly suggests that cytochrome P450IIB1 is a major contributor to the activation of aflatoxin B1 in rat hepatoma cells. The kind of strategy described here could be applied to other compounds that become cytotoxic for hepatoma cells following activation by cytochromes P450.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00633831
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    Paper (German National Licenses)
    Fulltext
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