Affiliation:
1. Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, New Hampshire 03755
Abstract
ABSTRACT
Activation of the
tcpPH
promoter on the
Vibrio
pathogenicity island by AphA and AphB initiates the
Vibrio cholerae
virulence cascade and is regulated by quorum sensing through the repressive action of HapR on
aphA
expression. To further understand how the chromosomally encoded AphA protein activates
tcpPH
expression, site-directed mutagenesis was used to identify the base pairs critical for AphA binding and transcriptional activation. This analysis revealed a region of partial dyad symmetry, TATGCA-N6-TNCNNA, that is important for both of these activities. Searching the
V. cholerae
genome for this binding site permitted the identification of a second one upstream of a penicillin V amidase (PVA) gene on the small chromosome. AphA binds to and footprints this site, which overlaps the
pva
transcriptional start, consistent with its role as a repressor at this promoter. Since
aphA
expression is under quorum-sensing control, the response regulators LuxO and HapR also influence
pva
expression. Thus,
pva
is repressed at low cell density when AphA levels are high, and it is derepressed at high cell density when AphA levels are reduced. Penicillin amidases are thought to function as scavengers for phenylacetylated compounds in the nonparasitic environment. That AphA oppositely regulates the expression of
pva
from that of virulence, together with the observation that PVA does not play a role in virulence, suggests that these activities are coordinated to serve
V. cholerae
in different biological niches.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
62 articles.
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