Regulation of glucosamine utilization in Staphylococcus aureus and Escherichia coli.
Glucosamine- or N-acetylglucosamine-requiring mutants of Staphylococcus aureus 209P and Escherichia coli K12, which lack glucosamine-6-phosphate synthetase [2-amino-2-deoxy-D-glucose-6-phosphate ketol-isomerase (amino-transferring); EC 5.3.1.19], were isolated. Growth of these mutants on glucosamine was inhibited by glucose, but growth on N-acetylglucosamine was not. Addition of glucose to mutant cultures growing exponentially on glucosamine inhibited growth and caused death of bacteria, though chloramphenicol prevented death. Uptake of glucosamine by S. aureus and E. coli mutants was severely inhibited by glucose whereas uptake of N-acetylglucosamine was only slightly inhibited. Uptake of glucose was not inhibited by either glucosamine or N-acetylglucosamine. In glucosamine auxotrophs, glucose causes glucosamine deficiency which interrupts cell wall synthesis and results in some loss of viability in the presence of continued protein synthesis.
D000117:Acetylglucosamine / Q000378:metabolism; D002701:Chloramphenicol / Q000494:pharmacology; D004926:Escherichia coli / Q000254:growth & development / Q000378:metabolism*; D005944:Glucosamine / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D010770:Phosphotransferases / Q000037:antagonists & inhibitors; D013211:Staphylococcus aureus / Q000254:growth & development / Q000378:metabolism*
D002701:Chloramphenicol; D010770:Phosphotransferases; D005947:Glucose; D005944:Glucosamine; D000117:Acetylglucosamine