J Bacteriol, May 1998, p. 2609-2615, Vol. 180, No. 10
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Department of Microbiology and Immunology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73190
Received 16 October 1997/Accepted 17 March 1998
Staphylococcus aureus KSI9051 has a complex mutation
that was associated with the aberrant expression of cell surface and extracellular proteins (M. S. Smeltzer, M. E. Hart, and
J. J. Iandolo, J. Bacteriol. 61:919-925, 1993). This mutation was
named xpr, although no specific gene was identified. Here
this mutation is referred to as
1058::Tn551.
In this study, we show that in strain KSI9051, the
1058::Tn551 mutation occurred
coincidentally with a frameshift in agrC that is
expected to truncate the sensor component of the known staphylococcal
global regulatory locus agr. Remarkably, pleiotropic
mutations affecting cell surface and extracellular proteins are
generated at frequencies approaching 50% upon the transduction of
erythromycin resistance (Emr) encoded by
1058::Tn551 from S. aureus KSI905
back to its parental strain, S6C. Three independent isolates created in
the manner of KSI9051 contained mutations within agrC. Each
isolate had different mutations, suggesting that the
transduction of Emr encoded by
1058::Tn551 affects the stability of
agrC in S6C. In similar experiments with strains from an
S. aureus 8325 genetic background, a mutant AgrC phenotype
could not be isolated, implying that strain S6 has aberrant genetic
behavior. A comparison of the nucleotide sequences of AgrC from several
strains revealed seven errors in the GenBank entry for agr
(X52543); these data were confirmed with plasmid pRN6650, the original
wild-type clone of agr.
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