Although a non-cytotoxic form of polymyxin B -- termed polymyxin B nonapeptide -- could partially protect a Salmonella pmrA mutant from Fe - mediated killing inactivation of the PmrA-activated loci responsible for the lipid-A modification with i.e. pbgP or phosphoethanolamine ( i.e. pmrC ) did not render the organism susceptible to Fe .
Although a non-cytotoxic form of polymyxin B -- termed polymyxin B nonapeptide -- could partially protect a Salmonella pmrA mutant from Fe - mediated killing inactivation of the PmrA-activated loci responsible for the lipid-A modification with 4-aminoarabinose or phosphoethanolamine ( i.e. pmrC ) did not render the organism susceptible to Fe .
Further support for PmrA pathways is the observation that inactivation of pmrA does not completely abolish the DrpoN-mediated PM resistance .
We have now determined that the regulatory protein PmrA is an antivirulence factor because inactivation of the pmrA gene exacerbated Salmonella virulence in Fig. 1A .
We have now determined that the regulatory protein PmrA is an antivirulence factor because inactivation of the pmrA gene exacerbated Salmonella virulence in C3H/HeN mice .