Open AccessLoss of secreted hemolysin activity in the mutant strain Hsb. 1 is due to a lesion in a plasmid copy number locus
Author(s) -
Diaz Pilar,
Hughes Colin,
Juárez Antonio
Publication year - 1991
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.1991.tb04388.x
Subject(s) - mutant , plasmid , hemolysin , locus (genetics) , biology , microbiology and biotechnology , strain (injury) , phenotype , genetics , virulence , chemistry , gene , anatomy
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.