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J. Bacteriol. doi:10.1128/JB.00972-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Interference of components of the PEP:phosphotransferase system (PTS) with the central virulence gene regulator PrfA of Listeria monocytogenes

Lehrstuhl für Mikrobiologie, Biozentrum, Universität Würzburg, D-97074 Würzburg, Germany; and Lehrstuhl für Mikrobiologie, Institut für Mikrobiologie, Biochemie und Genetik der Friedrich-Alexander Universität Erlangen-Nürnberg, D-91058 Erlangen, Germany

^* To whom correspondence should be addressed. Email: goebel{at}biozentrum.uni-wuerzburg.de,

	Abstract

Analysis of L. monocytogenes ptsH, hprK and ccpA mutants defective in carbon catabolite repression (CCR) control revealed significant alterations in the expression of PrfA-dependent genes. The hprK mutant showed high up-regulation of PrfA-dependent virulence genes upon growth in glucose-containing media whereas expression of these genes was even slightly down-regulated in the ccpA mutant when compared to the wild-type strain. The ptsH mutant could only grow in a rich culture medium and here the PrfA-dependent genes were up-regulated as in the hprK mutant. As expected, HPr-Ser-P was not produced in the hprK and ptsH mutants and synthesized at a similar level in the ccpA mutant as in the wild-type strain. However, no direct correlation was found between the level of HPr-Ser-P or HPr-His-P and PrfA activity when L. monocytogenes was grown in minimal medium with different PTS carbohydrates.

Comparison of the transcript profiles of the hprK and ccpA mutants with that of the wild-type strain indicates that the up-regulation of the PrfA-dependent virulence genes in the hprK mutant correlates with the down-regulation of genes known to be controlled by the efficiency of PTS-mediated glucose transport. Furthermore, growth in the presence of the non-PTS substrate glycerol results in high PrfA activity. These data suggest that not component(s) of the CCR or the common PTS pathway but rather of subsequent steps seem to be involved in the modulation of PrfA activity.

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