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  • 1
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    The hemolytic activity of heterocyclic N-alkyl amine oxides (1977)
    Springer
    Details
    Publication Date: 1977-11-01
    Print ISSN: 0014-4754
    Topics: Biology , Medicine
    Published by Springer
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  • 2
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    Mucidin Resistance in Yeast. Isolation, Characterization and Genetic Analysis of Nuclear and Mitochondrial Mucidin-Resistant Mutants of Saccharomyces cerevisiae (1977)
    Wiley
    Details
    Publication Date: 1977-02-01
    Print ISSN: 0014-2956
    Electronic ISSN: 1432-1033
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Wiley on behalf of Federation of European Biochemical Societies.
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  • 3
    Electronic Resource
    Electronic Resource
    The hemolytic activity of heterocyclic N-alkyl amine oxides (1977)
    Springer
    Cellular and molecular life sciences 33 (1977), S. 1415-1416 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The N-alkyl derivatives of morpholine-, pyrrolidine-, piperidine- and perhydroasepine-N-oxides caused the rapid, temperature-dependent, hemolysis of human red blood cells. The most hemolytic were the amine oxides with alkyl groups having 14–18 carbon atoms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01918776
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  • 4
    Electronic Resource
    Electronic Resource
    Genetic determination of ubiquinol-cytochromec reductase (1978)
    Springer
    Molecular genetics and genomics 161 (1978), S. 99-108 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary In order to find new genetic loci on the yeast mitochondrial DNA, especially mutations affecting the structure and function of ubiquinol-cytochrome c reductase, 45 independently arisen mutants resistant to mucidin have been isolated after MnCl2 mutagenesis. The majority of the mutants exhibited increased sensitivity to chloramphenicol, diuron and antimycin A, respectively. it was shown by several criteria that all mutants resulted from mutations localized on the mitochondrial DNA. The allelism tests revealed that these mutations fall into three distinct loci muc1, muc2 and muc3. Mutations at a new locus muc3 were correlated with the changes in the binding or inhibitory sites on the inner mitochondrial membrane. Multifactorial crosses involving the mucidin resistance mutations and mitochondrial mutations conferring resistance to chloramphenicol, erythromycin, oligomycin and diuron revealed that the studied mutations at the loci muc1, muc2 and muc3 did not significantly influence the process of mitochondrial recombination and its control by the mitochondrial locus ω. The locus muc1 was found to be allelic to the locus diu2. The locus muc2 which was found to be allelic to cob1 locus appears to be linked to the locus oli1 but unlinked to the loci ω, cap1, ery1 and muc1. The new locus muc3 appears to be weakly linked to the locus diu1 but unlinked to the loci ω, cap1, ery1, oli1 and muc1. The results are consistent with the gene order oli1-muc2-muc3-diu1-muc1-oli2 and suggest the participation of at least three mucidin resistance loci and one diuron resistance locus in the biogenesis of the bc 1 complex of the mitochondrial respiratory chain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00266620
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  • 5
    Electronic Resource
    Electronic Resource
    Localization of mucidin-resistant locus muc3 on mitochondrial DNA with respect to ubiquinol-cytochrome c reductase deficient box loci. Locus muc3 is allelic to box2 (1980)
    Springer
    Molecular genetics and genomics 179 (1980), S. 141-146 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Genetic relations between mitochondrial mucidin-resistant locus muc3 and ubiquinol-cytochrome c reductase-deficient box loci have been studied by recombination and petite deletion analysis. It was found that the locus muc3 maps in the segment of mitochondrial DNA corresponding to the locus box2. The results suggest the participation of box2/muc3 locus in the sequences of the structural gene for cytochrome b.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00268456
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  • 6
    Electronic Resource
    Electronic Resource
    Intramitochondrial ATP and cell functions (1978)
    Springer
    Molecular genetics and genomics 166 (1978), S. 103-116 
    Details
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Cells of Saccharomyces cerevisiae were depleted of intramitochondrial ATP by growing on a glucose-containing medium in the presence of antimycin A and bogkrekic acid. Antimycin A prevented ATP synthesis inside mitochondria by oxidative phosphorylation and bongkrekic acid inhibited import of glycol ytically-produced ATP from the cytosol into mitochondria. Growth of the cells containing ATP depleted mitochondria was accompanied by the following events 1. Mitochondrial genes were being continually lost from growing cells. The loss was random independently of whether the genes were located in the polar or the non-polar regions of the mitochondrial genome. 2. The growing cells were being continuously converted into cytoplasmic respiration-deficient (petite) mutants. The number of mutants was raising rapidly and could be expressed as a power function of the total number of cells. 3. Most of the ensuing petite mutants retained some of their mitochondrial genetic markers and suppressed the respiration-competent genotype in diploids which had been formed in crosses of the mutants with wild-type strains. This indicates that the mutants contained mitochondrial DNA and could not be produced as a suit of a simple dilution of mitochondrial DNA out of the cells lacking intramitochondrial ATP. 4. When the growing cells lacking intramitochondrial ATP were crossed to strains which had not been energy-depleted transmission of mitochondrial genes from the depleted cells and frequency of recombinants were generally diminishing in accord with the assumption that the shortage in intramitochondrial energy led to decrease in input of mitochondrial alleles into the common mating pool. 4. No respiration-deficient mutants were formed in culture of cells lacking intramitochondrial ATP under non-growing conditions. The events may be accounted for as a reaction of mitochondria to starvation for an energy source consisting in multiple random excisions of genes from the complete genophore in the form of elements that could spread away, replicate and reinsert into other genophores. The process may be considered as a remnant of an adaptive response of a common gene pool to a situation of emergency.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00379735
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