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J Bacteriol. 1971 July; 107(1): 245-250
Copyright © 1971 American Society for Microbiology. All Rights Reserved.
Departments of Medical Microbiology, Microbiology, and Pharmaceutical Biochemistry, University of Uppsala, Uppsala, Sweden
ABSTRACT
Staphylococcus aureus Cowan I was exposed to nitrosoguanidine or ethyl-methanesulfonate, and survivors were screened on nutrient agar plates containing rabbit anti-protein A serum for loss of protein A production. More than half of all protein A-deficient mutants also lacked nuclease, coagulase, alpha hemolysin, fibrinolysin, mannitol utilization, and the phage-type pattern. Mutants with a spectrum of these properties were also isolated. Induced or spontaneous reversions of the mutants were observed. The properties of the protein A-deficient mutants suggest that synthesis or release (or both) of a number of extracellular products of S. aureus is controlled by a common regulatory mechanism.
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