Abstract
Three mitomycin-C-sensitive (MC s) strains of Haemophilus influenzae, being poorly transformable with DNA carrying the antibiotic resistence markers nov r and ery r, were further investigated to determine the cause of their poor transformability. After being genetically integrated into the mutant-recipient genome the donor marker is replicated at the same rate as in the wild type, indicating that recombination in the mutant strains is normal. In the mutants, designated T d (transformation-deficient), the poor transformability for the nov r and ery r markers is due to the lack of phenotypic expression of the markers, because the strains are killed by concentrations of antibiotics normally used to select for nov r and ery r transformants. Since the strains exhibit extreme sensitivity both to deoxycholate and osmotic shock in the presence of EDTA, the increased sensitivity to antibiotics (including mitomycin-C) is probably caused by a change in the cell envelope. Although recombination in the mutant strains proceeds normally, the T d mutation nevertheless decreases both the rate of inactivation and of integration of donor DNA.
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More From: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
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