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Transcriptional Regulation and PosttranslationalActivity of the Betaine Transporter BetL in Listeriamonocytogenes Are Controlled by EnvironmentalSalinity
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ABSTRACT
While
the genetic elements contributing to the salinity tolerance of
Listeria monocytogenes
have been well characterized, the
regulatory signals and responses (genetic and/or biochemical) that
govern these mechanisms have yet to be elucidated. Encoded by
betL
, the first genetic element to be linked to listerial
osmotolerance, the secondary betaine uptake system BetL is a member of
the betaine-carnitine-choline transporter family. Preceded by consensusσ
A
- and σ
B
-dependent promoter
sites,
betL
is constitutively expressed and transcriptionally
up-regulated in response to salt stress. The nisin-controlled
expression system was used to achieve salinity-independent, controlled
betL
expression in
Listeria
. In the absence of
NaCl-activated transcriptional control, BetL activity was found to be a
function of environmental salinity, showing optimal activity in buffer
supplemented with 1 to 2% NaCl (osmolality, 417 to 719
mosmol/kg). In addition, BetL was activated rapidly (half-life, 2 min)
in response to an osmotic upshift imposed by adding 2% NaCl to
50 mM potassium phosphate
buffer.
American Society for Microbiology
Title: Transcriptional Regulation and PosttranslationalActivity of the Betaine Transporter BetL in
Listeriamonocytogenes
Are Controlled by EnvironmentalSalinity
Description:
ABSTRACT
While
the genetic elements contributing to the salinity tolerance of
Listeria monocytogenes
have been well characterized, the
regulatory signals and responses (genetic and/or biochemical) that
govern these mechanisms have yet to be elucidated.
Encoded by
betL
, the first genetic element to be linked to listerial
osmotolerance, the secondary betaine uptake system BetL is a member of
the betaine-carnitine-choline transporter family.
Preceded by consensusσ
A
- and σ
B
-dependent promoter
sites,
betL
is constitutively expressed and transcriptionally
up-regulated in response to salt stress.
The nisin-controlled
expression system was used to achieve salinity-independent, controlled
betL
expression in
Listeria
.
In the absence of
NaCl-activated transcriptional control, BetL activity was found to be a
function of environmental salinity, showing optimal activity in buffer
supplemented with 1 to 2% NaCl (osmolality, 417 to 719
mosmol/kg).
In addition, BetL was activated rapidly (half-life, 2 min)
in response to an osmotic upshift imposed by adding 2% NaCl to
50 mM potassium phosphate
buffer.
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