Affiliation:
1. Program in Molecular Pathogenesis, Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, and Departments of Microbiology and Medicine, New York University Medical Center, New York, New York 10016
2. Department of Microbiology Tumor and Cell Biology, Karolinska Institute, S 171 77 Stockholm, Sweden
Abstract
ABSTRACT
TraP is a triply phosphorylated staphylococcal protein that has been hypothesized to be the mediator of a second
Staphylococcus aureus
quorum-sensing system, “SQS1,” that controls expression of the
agr
system and therefore is essential for the organism's virulence. This hypothesis was based on the loss of
agr
expression and virulence by a
traP
mutant of strain 8325-4 and was supported by full complementation of both phenotypic defects by the cloned
traP
gene in strain NB8 (Y. Gov, I. Borovok, M. Korem, V. K. Singh, R. K. Jayaswal, B. J. Wilkinson, S. M. Rich, and N. Balaban, J. Biol. Chem. 279:14665-14672, 2004), in which the wild-type
traP
gene was expressed in
trans
in the 8325-4
traP
mutant. We initiated a study of the mechanism by which TraP activates
agr
and found that the
traP
mutant strain used for this and other recently published studies has a second mutation, an adventitious stop codon in the middle of
agrA
, the
agr
response regulator. The
traP
mutation, once separated from the
agrA
defect by outcrossing, had no effect on
agr
expression or virulence, indicating that the
agrA
defect accounts fully for the lack of
agr
expression and for the loss of virulence attributed to the
traP
mutation. In addition, DNA sequencing showed that the
agrA
gene in strain NB8 (Gov et al., J. Biol. Chem., 2004), in contrast to that in the
agr
-defective 8325-4
traP
mutant strain, had the wild-type sequence; further, the
traP
mutation in that strain, when outcrossed, also had no effect on
agr
expression.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
60 articles.
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