Regulation of staphylococcal enterotoxin B.
The effect of glucose and the glucose analogues 2-deoxyglucose and alpha-methyl-glucoside on the synthesis and regulation of staphylococcal enterotoxin B was examined. The attenuating effect of glucose on staphylococcal enterotoxin B synthesis was observed. However, when this effect was examined with analogues of glucose, contradictory responses were seen. alpha-Methylglucoside had a slight stimulatory effect on enterotoxin production and other extracellular proteins, whereas 2-deoxyglucose markedly inhibited enterotoxin production. beta-hemolysin and staphylococcal nuclease were also inhibited by 2-deoxy glucose but the synthesis of nuclease could be rescued by the addition of glucose to 2-deoxyglucose-containing cultures. Enterotoxin and beta-hemolysin synthesis were not subject to glucose rescue. The cells used in this study were permeable to cyclic 3',5'-adenosine monophosphate, but the addition of this compound did not reverse glucose repression or 2-deoxyglucose inhibition of enterotoxin B synthesis. We conclude from these data that the regulation of enterotoxin is not under catabolite control as previously reported.[1]References
- Regulation of staphylococcal enterotoxin B. Iandolo, J.J., Shafer, W.M. Infect. Immun. (1977) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg









