Affiliation:
1. Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, North Carolina 27858,1 and
2. Department of Microbiology and Immunology, University of Rochester School of Medicine, Rochester, New York 146422
Abstract
ABSTRACT
The opportunistic pathogen
Pseudomonas aeruginosa
uses intercellular signals to control the density-dependent expression of many virulence factors. The
las
and
rhl
quorum-sensing systems function, respectively, through the autoinducers
N
-(3-oxododecanoyl)-
l
-homoserine lactone and
N
-butyryl-
l
-homoserine lactone (C
4
-HSL), which are known to positively regulate the transcription of the elastase-encoding gene,
lasB
. Recently, we reported that a second type of intercellular signal is involved in
lasB
induction. This signal was identified as 2-heptyl-3-hydroxy-4-quinolone and designated the
Pseudomonas
quinolone signal (PQS). PQS was determined to be part of the quorum-sensing hierarchy since its production and bioactivity depended on the
las
and
rhl
quorum-sensing systems, respectively. In order to define the role of PQS in the
P. aeruginosa
quorum-sensing cascade,
lacZ
gene fusions were used to determine the effect of PQS on the transcription of the quorum-sensing system genes
lasR
,
lasI
,
rhlR
, and
rhlI
. We found that in
P. aeruginosa
, PQS caused a major induction of
rhlI′-lacZ
and had lesser effects on the transcription of
lasR′-lacZ
and
rhlR′-lacZ
. We also observed that the transcription of both
rhlI′-lacZ
and
lasB′-lacZ
was cooperatively effected by C
4
-HSL and PQS. Additionally, we present data indicating that PQS was not produced maximally until cultures reached the late stationary phase of growth. Taken together, our results imply that PQS acts as a link between the
las
and
rhl
quorum-sensing systems and that this signal is not involved in sensing cell density.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
321 articles.
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