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Department of Food Science, Cornell University, Ithaca, New York 14853, USA
* To whom correspondence should be addressed. Email:
kjb4{at}cornell.edu.
Some Listeria monocytogenes internalins are recognized as contributing to invasion of mammalian tissue culture cells. While PrfA is well-established as a positive regulator of L. monocytogenes virulence gene expression, the stress responsive
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
The alternative sigma factor
B and the virulence gene regulator PrfA both regulate transcription of Listeria monocytogenes internalins
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Abstract
B has been recognized only recently as contributing to expression of virulence genes, including some that encode internalins. To measure the relative contributions of PrfA and
B to internalin gene transcription, we used RT-PCR to quantify transcript levels for eight internalin genes (inlA, inlB, inlC, inlC2, inlD, inlE, inlF and inlG) in L. monocytogenes 10403S and in isogenic
prfA,
sigB and
sigB
prfA strains. Strains were grown under defined conditions to produce (i) active PrfA; (ii) active
B and active PrfA; (iii) inactive PrfA; and (iv) active
B and inactive PrfA. Under the conditions tested,
B and PrfA contributed differentially to expression of the various internalins such that (i) both
B and PrfA contributed to inlA and inlB transcription, (ii) only PrfA contributed to inlC transcription, (iii) only
B contributed to inlC2 and inlD transcription, and (iv) neither
B nor PrfA contributed to inlF and inlG transcription. Transcript levels were undetectable for inlE. The important role for
B in regulating expression of L. monocytogenes internalins suggests that exposure of this organism to environmental stress conditions, such as those encountered in the gastrointestinal tract, may activate internalin transcription. Interplay between
B and PrfA also appears to be critical for regulating transcription of some virulence genes, including inlA, inlB, and prfA.
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