SUMMARY: Mutant staphylococci with impaired respiration, induced by ultraviolet radiation, were used for testing various inhibitors with already known mechanisms of action. Inhibitors of protein synthesis (the tetracyclins) affected the growth of parent and mutant cultures to the same degree. To the inhibitors of cell-wall synthesis (the penicillins) mutant staphylococci were more resistant than the parents; this was related to the altered amino acid composition of cell-wall material in the mutants. On the other hand, the mutants were much more vulnerable than parents to the action of inhibitors which affected the nucleic acids—namely, mitomycin C (x 50 times), actinomycin C (x 50). trypaflavine (x 300), nitrogen mustards (x 10-20). A specific thymine synthetase inhibitor (5-fluorodeoxyuridine) strongly inhibited the growth of parent staphylococci, but did not at all inhibit the growth of mutants. This points to some deficiency in the enzymic mechanism of synthesis of thymine in the DNA of mutants. Experiments with 5-bromodeoxyuridine suggest that the mutant staphylococci lacked the enzymic mechanism necessary for effective incorporation of halogenated pyrimidines into the DNA precursor pool.


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