Department of Microbiology and Alimentary Pharmabiotic Centre, University College, Cork, Ireland,1 Department of Microbiology, University of Guelph, Guelph, Ontario, Canada N1G 2W12
Received 2 July 2003/ Accepted 15 September 2003
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 consensus
A- and
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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