Further studies have been carried out on mutation hsb which was previously suggested to block hemolysin secretion (Muñoa et al., 1988, FEMS Microbiol. Lett. 56: 167-172). We show that the reported reduction in the extracellular hemolytic activity of mutant Hsb. 1 is due to lower hemolysin synthesis and that this is itself a consequence of a decrease in plasmid copy number. We suggest that the hsb is identical to the pcnB lesion located at minute 3.6 of the chromosome.
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Dı́az et al. (1991) studied this question.
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