Glucose-1-phosphate utilization by Listeria monocytogenes is PrfA dependent and coordinately expressed with virulence factors

Maria Teresa Ripio, Klaus Brehm, Maria Lara, Maria Suarez, Jose A Vazquez-Boland

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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. We found that prfA* mutants that constitutively overexpress the virulence regulon due to a Gly145Ser substitution in PrfA (M.-T. Ripio, G. Domínguez-Bernal, M. Lara, M. Suárez, and J.-A. Vázquez-Boland, J. Bacteriol. 179:1533-1540, 1997) rapidly utilized glucose-1-phosphate (G-1-P) as a carbon source for growth, in contrast to wild-type strains, which characteristically do not. Wild-type strains acquired the capacity for readily metabolizing G-1-P upon exposure to environmental conditions that activate the expression of prfA and PrfA-dependent virulence genes (i.e., culture at 37 degrees C in charcoal-treated medium). In these strains, G-1-P utilization followed an expressional pattern identical to that of virulence genes controlled by PrfA, with repression at 20 degrees C. Tn917 insertions in L. monocytogenes mutants selected for G-1-P utilization deficiency mapped to the plcA-prfA operon, a deltaprfA strain was totally unable to utilize G-1-P, and trans complementation with prfA constructs restored the ability to efficiently metabolize and grow on G-1-P to these mutants. Thus, G-1-P utilization by L. monocytogenes is under the tight positive control of the central virulence regulator, PrfA, and is coexpressed with PrfA-dependent pathogenicity determinants. It was recently reported that readily utilized carbohydrates, such as glucose or cellobiose, repress virulence genes in L. monocytogenes. We confirmed this but, interestingly, found that G-1-P does not inhibit expression of the PrfA regulon, indicating that this sugar follows a catabolic pathway that bypasses the repressor mechanism triggered by other readily metabolized carbon sources. PrfA dependence and coexpression with virulence genes suggest that utilization of exogenous G-1-P may be relevant to Listeria pathogenesis. G-1-P is the precursor metabolite and primary degradation product of glycogen and is therefore available within the mammalian cell. Based on our results, we hypothesize that G-1-P could play an important role as a growth substrate for intracellular Listeria.
Original languageEnglish
Pages (from-to)7174-80
Number of pages7
JournalJournal of Bacteriology
Issue number22
Publication statusPublished - Nov 1997

Keywords / Materials (for Non-textual outputs)

  • Amino Acid Substitution
  • Bacterial Proteins/genetics
  • Bacterial Proteins/metabolism
  • Cellobiose/metabolism
  • Chromosome Mapping
  • DNA Transposable Elements
  • Gene Expression Regulation, Bacterial
  • Glucose/metabolism
  • Glucosephosphates/metabolism
  • Listeria monocytogenes/genetics
  • Listeria monocytogenes/metabolism
  • Listeria monocytogenes/pathogenicity
  • Mutagenesis, Insertional
  • Peptide Termination Factors
  • Regulon
  • Trans-Activators/genetics
  • Trans-Activators/metabolism
  • Virulence/genetics


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