Enterotoxin A synthesis in Staphylococcus aureus: inhibition by glycerol and maltose.
Studies indicated that prior growth of Staphylococcus aureus 196E on glycerol or maltose led to cells with repressed ability to produce staphylococcal enterotoxin A (SEA). A PTS- mutant (196E-MA) lacking the phosphoenolpyruvate phosphotransferase system (PTS), derived from strain 196E, showed considerably less repression of SEA synthesis when cells were grown in glycerol or maltose. Since SEA synthesis is not repressed in the PTS- mutant, repression of toxin synthesis by glycerol, maltose or glucose in S. aureus 196E appears to be related to the presence of a functional PTS irrespective of whether the carbohydrate requires the PTS for cell entry. With lactose as an inducer, glucose, glycerol, maltose or 2-deoxyglucose repressed the synthesis of beta-galactosidase in S. aureus 196E. It is postulated that these compounds repress enzyme synthesis by an inducer exclusion mechanism involving phosphorylated sugar intermediates. However, inducer exclusion probably does not explain the mechanism of repression of SEA synthesis by carbohydrates.
D004768:Enterotoxins / Q000096:biosynthesis*; D004794:Enzyme Repression; D005947:Glucose / Q000378:metabolism; D005990:Glycerol / Q000494:pharmacology*; D008320:Maltose / Q000494:pharmacology*; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System / Q000502:physiology; D013211:Staphylococcus aureus / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D000520:alpha-Glucosidases / Q000096:biosynthesis; D001616:beta-Galactosidase / Q000096:biosynthesis
D004768:Enterotoxins; C026066:enterotoxin A, Staphylococcal; D008320:Maltose; D010731:Phosphoenolpyruvate Sugar Phosphotransferase System; D000520:alpha-Glucosidases; D001616:beta-Galactosidase; D005947:Glucose; D005990:Glycerol