Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Gene Review:

prfA - listeriolysin positive regulatory protein

Listeria monocytogenes EGD-e

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of prfA

Virulence genes of the facultative intracellular pathogen Listeria monocytogenes are coordinately regulated by the activator protein PrfA, encoded by prfA, a member of the cyclic AMP receptor protein family of bacterial transcription factors [1].

Psychiatry related information on prfA

Intraspecific phylogeny and lineage group identification based on the prfA virulence gene cluster of Listeria monocytogenes [2].

High impact information on prfA

This study identifies a second key virulence regulon in L. monocytogenes, after the prfA regulon [3].
Comparative transcriptome analyses were performed with RNA isolated from a prfA mutant and an isogenic strain carrying multiple copies of prfA or prfA* on a plasmid [4].
This substitution inactivated PrfA, since expression of the PrfAK220T mutant gene in an EGDDeltaprfA strain did not restore the haemolytic and phosphatidylcholine phospholipase C activities, in contrast to the wild-type prfA gene [5].
The sequencing of prfA, encoding the transcriptional regulator of virulence genes, in 26 low-virulence field Listeria monocytogenes strains showed that eight strains exhibited the same single amino-acid substitution: PrfAK220T [5].
Increased plcA transcript levels, which were similar in both host cell vacuole and cytosol, were associated with increases in both prfA expression and PrfA activity. qRT-PCR assays were designed to measure expression of prfA from each of its three promoter regions [6].

Chemical compound and disease context of prfA

Virulence genes in Listeria monocytogenes are coordinately expressed under the control of the transcriptional activator PrfA, encoded by prfA, a member of the cyclic AMP (cAMP) receptor protein (CRP)/FNR family of bacterial regulators [7].

Biological context of prfA

In summary (i) sigmaB is primarily activated during environmental stress and does not contribute to PrfA activation in intracellular L. monocytogenes and (ii) the partially sigmaB-dependent P2prfA promoter region contributes the majority of prfA transcripts in both intra- and extracellular bacteria [6].
In order to test hypotheses regarding L. monocytogenes lineage composition, evolution, ecology, and taxonomy, a robust intraspecific phylogeny was developed based on prfA virulence gene cluster sequences from 113 L. monocytogenes isolates [2].

Other interactions of prfA

To determine whether any host responses were due to recognition of specific virulence factors during infection, we also examined the transcriptional response to two bacterial mutants; actA which is defective in actin-based motility, and prfA, which is defective in the expression of all L. monocytogenes virulence genes [8].

Analytical, diagnostic and therapeutic context of prfA

Detection of Listeria monocytogenes in food using a combined enrichment/real-time PCR method targeting the prfA gene [9].
By using murine macrophage-like J774.1 cells with or without activation by IFN-gamma plus LPS, the expression of both hly and its positive regulator prfA was monitored by means of RT-PCR [10].

References

Glucose-1-phosphate utilization by Listeria monocytogenes is PrfA dependent and coordinately expressed with virulence factors. Ripio, M.T., Brehm, K., Lara, M., Suárez, M., Vázquez-Boland, J.A. J. Bacteriol. (1997) [Pubmed]
Intraspecific phylogeny and lineage group identification based on the prfA virulence gene cluster of Listeria monocytogenes. Ward, T.J., Gorski, L., Borucki, M.K., Mandrell, R.E., Hutchins, J., Pupedis, K. J. Bacteriol. (2004) [Pubmed]
VirR, a response regulator critical for Listeria monocytogenes virulence. Mandin, P., Fsihi, H., Dussurget, O., Vergassola, M., Milohanic, E., Toledo-Arana, A., Lasa, I., Johansson, J., Cossart, P. Mol. Microbiol. (2005) [Pubmed]
Overexpression of PrfA leads to growth inhibition of Listeria monocytogenes in glucose-containing culture media by interfering with glucose uptake. Marr, A.K., Joseph, B., Mertins, S., Ecke, R., Müller-Altrock, S., Goebel, W. J. Bacteriol. (2006) [Pubmed]
A naturally occurring mutation K220T in the pleiotropic activator PrfA of Listeria monocytogenes results in a loss of virulence due to decreasing DNA-binding affinity. Velge, P., Herler, M., Johansson, J., Roche, S.M., Témoin, S., Fedorov, A.A., Gracieux, P., Almo, S.C., Goebel, W., Cossart, P. Microbiology (Reading, Engl.) (2007) [Pubmed]
Contributions of Listeria monocytogenes sigmaB and PrfA to expression of virulence and stress response genes during extra- and intracellular growth. Kazmierczak, M.J., Wiedmann, M., Boor, K.J. Microbiology (Reading, Engl.) (2006) [Pubmed]
A Gly145Ser substitution in the transcriptional activator PrfA causes constitutive overexpression of virulence factors in Listeria monocytogenes. Ripio, M.T., Domínguez-Bernal, G., Lara, M., Suárez, M., Vazquez-Boland, J.A. J. Bacteriol. (1997) [Pubmed]
A gene-expression program reflecting the innate immune response of cultured intestinal epithelial cells to infection by Listeria monocytogenes. Baldwin, D.N., Vanchinathan, V., Brown, P.O., Theriot, J.A. Genome Biol. (2003) [Pubmed]
Detection of Listeria monocytogenes in food using a combined enrichment/real-time PCR method targeting the prfA gene. Rossmanith, P., Krassnig, M., Wagner, M., Hein, I. Res. Microbiol. (2006) [Pubmed]
Involvement of reactive oxygen intermediate in the enhanced expression of virulence-associated genes of Listeria monocytogenes inside activated macrophages. Makino, M., Kawai, M., Kawamura, I., Fujita, M., Gejo, F., Mitsuyama, M. Microbiol. Immunol. (2005) [Pubmed]

Contributions to this collaborative article are from individual authors of WikiGenes or mined by the WikiGenes Data Mining Engine from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.