Induction of mutation in Staphylococcus aureus by ethylmethane sulphonate.
Staphylococcus aureus strains were treated with ethylmethane sulphonate with the object of obtaining mutants that differed from the wild type in one of the properties that might contribute to virulence. Mutants with isolated loss or deficient production of gamma-haemolysin, coagulase, leucocidin and staphylokinase were obtained. Changes in more than one property were often observed. The loss of delta-lysin production was always coupled with an appreciable reduction in P-V leucocidin production. With that exception, systematised combined loss of a restricted number of staphylococcal characteristics was not observed. Mutants that had lost all characteristics of S. aureus were phage-resistant. Isolated loss of staphylokinase production and deficient P-V leucocidin production were found to be due to the independent loss of two prophages.
D000818:Animals; D001434:Bacteriophage Typing; D003030:Coagulase / Q000096:biosynthesis; D005020:Ethyl Methanesulfonate / Q000494:pharmacology*; D005341:Fibrinolysin / Q000096:biosynthesis; D006460:Hemolysin Proteins / Q000096:biosynthesis / Q000378:metabolism; D006801:Humans; D007956:Leukocidins / Q000096:biosynthesis; D008698:Mesylates / Q000494:pharmacology*; D051379:Mice; D009153:Mutagens; D009154:Mutation; D013045:Species Specificity; D013210:Staphylococcus / Q000201:enzymology / Q000378:metabolism* / Q000472:pathogenicity; D013204:Staphylococcus Phages
D003030:Coagulase; D006460:Hemolysin Proteins; D007956:Leukocidins; D008698:Mesylates; D009153:Mutagens; D005020:Ethyl Methanesulfonate; D005341:Fibrinolysin