Loss of secreted hemolysin activity in the mutant strain Hsb. 1 is due to a lesion in a plasmid copy number locus.
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.
Diaz
P
P
Department of Pathology, Cambridge University, U.K.
Hughes
C
C
Juárez
A
A
D002876:Chromosomes, Bacterial; D004269:DNA, Bacterial / Q000235:genetics / Q000302:isolation & purification; D004926:Escherichia coli / Q000235:genetics*; D006460:Hemolysin Proteins / Q000096:biosynthesis / Q000235:genetics* / Q000302:isolation & purification; D016254:Mutagenesis, Insertional; D010957:Plasmids
D004269:DNA, Bacterial; D006460:Hemolysin Proteins