AsnB is responsible for peptidoglycan precursor amidation in in the presence of vancomycin.

630 possesses a cryptic but functional gene cluster homologous to the operon of . Expression of in the presence of subinhibitory concentrations of vancomycin is accompanied by peptidoglycan amidation on the -DAP residue. In this paper, we report the presence of two potential asparagine synthetase genes named and in the genome whose products were potentially involved in this peptidoglycan structure modification. We found that expression was only induced when was grown in the presence of vancomycin, yet independently from the resistance and regulation operons. In addition, peptidoglycan precursors were not amidated when was inactivated. No change in vancomycin MIC was observed in the mutant strain. In contrast, overexpression of resulted in the amidation of most of the peptidoglycan precursors and in a weak increase of vancomycin susceptibility. AsnB activity was confirmed in . In contrast, the expression of the second asparagine synthetase, AsnB2, was not induced in the presence of vancomycin. In summary, our results demonstrate that AsnB is responsible for peptidoglycan amidation of in the presence of vancomycin.