Resistance of Streptococcus pneumoniaeto Deformylase Inhibitors Is Due to Mutations indefB
P Margolis, C Hackbarth, S Lopez… - Antimicrobial agents …, 2001 - Am Soc Microbiol
P Margolis, C Hackbarth, S Lopez, M Maniar, W Wang, Z Yuan, R White, J Trias
Antimicrobial agents and chemotherapy, 2001•Am Soc MicrobiolResistance to peptide deformylase inhibitors in Escherichia coli or Staphylococcus aureus is
due to inactivation of transformylase activity. Knockout experiments in Streptococcus
pneumoniae R6x indicate that the transformylase (fmt) and deformylase (defB) genes are
essential and that a def paralog (defA) is not. Actinonin-resistant mutants of S. pneumoniae
ATCC 49619 harbor mutations in defB but not in fmt. Reintroduction of the mutated defB
gene into wild-type S. pneumoniae R6x recreates the resistance phenotype. The altered …
due to inactivation of transformylase activity. Knockout experiments in Streptococcus
pneumoniae R6x indicate that the transformylase (fmt) and deformylase (defB) genes are
essential and that a def paralog (defA) is not. Actinonin-resistant mutants of S. pneumoniae
ATCC 49619 harbor mutations in defB but not in fmt. Reintroduction of the mutated defB
gene into wild-type S. pneumoniae R6x recreates the resistance phenotype. The altered …
Abstract
Resistance to peptide deformylase inhibitors in Escherichia coli or Staphylococcus aureus is due to inactivation of transformylase activity. Knockout experiments in Streptococcus pneumoniae R6x indicate that the transformylase (fmt) and deformylase (defB) genes are essential and that adef paralog (defA) is not. Actinonin-resistant mutants of S. pneumoniae ATCC 49619 harbor mutations indefB but not in fmt. Reintroduction of the mutated defB gene into wild-type S. pneumoniaeR6x recreates the resistance phenotype. The altered enzyme displays decreased sensitivity to actinonin.
American Society for Microbiology