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Gene Review

prgQ  -  peptide inhibitor iCF10

Enterococcus faecalis

 
 
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Disease relevance of prgQ

 

High impact information on prgQ

  • Results confirmed the 5' end of a very abundant, constitutively produced transcript (from prgQ) that had been mapped previously by primer extension and defined the initiation point of a less abundant, divergently transcribed message (from prgX) [2].
  • We propose a new model for the mechanism used by PrgX for regulation of the prgQ promoter, PrgX autoregulation, and Qa RNA processing [3].
  • Characterization of cis-acting prgQ mutants: evidence for two distinct repression mechanisms by Qa RNA and PrgX protein in pheromone-inducible enterococcal plasmid pCF10 [4].
  • However, both Qa RNA and PrgX protein were reduced in three Qa promoter region mutants and the expression of prgQ transcripts extending 3' from IRS1 became constitutive [4].
  • In this study, we isolated 14 single amino acid substitutions in PrgX that reduced or eliminated repression of prgQ, without affecting autoregulation or DNA binding [3].
 

Biological context of prgQ

 

Other interactions of prgQ

  • Neither production of this peptide nor translation of the 5' end of prgQ transcripts was found to be necessary for prgB expression [7].
  • Genes required for Asc10 production, prgQ and prgS, lie 3-5 kb upstream, but can function at much greater distances [7].
 

Analytical, diagnostic and therapeutic context of prgQ

  • Western blot (immunoblot) analysis of these mutants shows that prgQ is also essential for the expression of prgA (encoding the surface exclusion protein Sec10), which is located between prgB and the positive-control region [8].

References

  1. The prgQ gene of the Enterococcus faecalis tetracycline resistance plasmid pCF10 encodes a peptide inhibitor, iCF10. Nakayama, J., Ruhfel, R.E., Dunny, G.M., Isogai, A., Suzuki, A. J. Bacteriol. (1994) [Pubmed]
  2. Sensitive detection of bacterial transcription initiation sites and differentiation from RNA processing sites in the pheromone-induced plasmid transfer system of Enterococcus faecalis. Bensing, B.A., Meyer, B.J., Dunny, G.M. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  3. Enterococcus faecalis pheromone-responsive protein PrgX: genetic separation of positive autoregulatory functions from those involved in negative regulation of conjugative plasmid transfer. Kozlowicz, B.K., Bae, T., Dunny, G.M. Mol. Microbiol. (2004) [Pubmed]
  4. Characterization of cis-acting prgQ mutants: evidence for two distinct repression mechanisms by Qa RNA and PrgX protein in pheromone-inducible enterococcal plasmid pCF10. Bae, T., Kozlowicz, B.K., Dunny, G.M. Mol. Microbiol. (2004) [Pubmed]
  5. Two targets in pCF10 DNA for PrgX binding: their role in production of Qa and prgX mRNA and in regulation of pheromone-inducible conjugation. Bae, T., Kozlowicz, B., Dunny, G.M. J. Mol. Biol. (2002) [Pubmed]
  6. Analysis of expression of prgX, a key negative regulator of the transfer of the Enterococcus faecalis pheromone-inducible plasmid pCF10. Bae, T., Clerc-Bardin, S., Dunny, G.M. J. Mol. Biol. (2000) [Pubmed]
  7. Pheromone cCF10 and plasmid pCF10-encoded regulatory molecules act post-transcriptionally to activate expression of downstream conjugation functions. Bensing, B.A., Manias, D.A., Dunny, G.M. Mol. Microbiol. (1997) [Pubmed]
  8. Genetic analysis of a region of the Enterococcus faecalis plasmid pCF10 involved in positive regulation of conjugative transfer functions. Chung, J.W., Bensing, B.A., Dunny, G.M. J. Bacteriol. (1995) [Pubmed]
 
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