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Enterotoxin A synthesis in Staphylococcus aureus: inhibition by glycerol and maltose

J L Smith1, M M Bencivengo, C A Kunsch

  • 1United States Department of Agriculture, Philadelphia, PA 19118.

Journal of General Microbiology
|December 1, 1986
PubMed

Insights

Staphylococcus aureus toxin production (SEA) is repressed by certain sugars, but this repression is linked to the phosphoenolpyruvate phosphotransferase system (PTS). A mutant lacking PTS shows less repression, suggesting PTS function is key for sugar-mediated SEA synthesis control.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Pathogenesis

Background:

  • Staphylococcus aureus produces staphylococcal enterotoxin A (SEA), a significant foodborne illness agent.
  • Carbohydrate metabolism in bacteria often influences the production of virulence factors.
  • The phosphoenolpyruvate phosphotransferase system (PTS) is crucial for sugar uptake and metabolism in many bacteria.

Purpose of the Study:

  • To investigate the role of the phosphoenolpyruvate phosphotransferase system (PTS) in the regulation of staphylococcal enterotoxin A (SEA) synthesis by carbohydrates in Staphylococcus aureus.
  • To determine if PTS-dependent or PTS-independent mechanisms mediate carbohydrate-induced repression of SEA production.

Main Methods:

  • Growth of Staphylococcus aureus strain 196E and a derived PTS- mutant (196E-MA) on various carbohydrates (glycerol, maltose, glucose, lactose).
  • Quantification of staphylococcal enterotoxin A (SEA) production under different growth conditions.
  • Assay of beta-galactosidase synthesis in the presence of lactose and other carbohydrates to study inducer exclusion mechanisms.

Main Results:

  • Prior growth of S. aureus 196E on glycerol or maltose repressed SEA production.
  • A PTS- mutant (196E-MA) exhibited significantly reduced repression of SEA synthesis when grown on glycerol or maltose.
  • Glucose, glycerol, maltose, and 2-deoxyglucose repressed beta-galactosidase synthesis in the presence of lactose, suggesting inducer exclusion.
  • Repression of SEA synthesis by carbohydrates was not observed in the PTS- mutant, indicating a role for a functional PTS.

Conclusions:

  • The presence of a functional phosphoenolpyruvate phosphotransferase system (PTS) is critical for the repression of staphylococcal enterotoxin A (SEA) synthesis by carbohydrates in Staphylococcus aureus.
  • Carbohydrate-mediated repression of SEA synthesis appears to be linked to PTS activity, irrespective of the specific carbohydrate's entry mechanism.
  • The mechanism of SEA repression by carbohydrates likely differs from the inducer exclusion mechanism observed for beta-galactosidase synthesis.

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