In:
Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 45, No. 9 ( 2001-09), p. 2432-2435
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 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 enzyme displays decreased sensitivity to actinonin.
Type of Medium:
Online Resource
ISSN:
0066-4804
,
1098-6596
DOI:
10.1128/AAC.45.9.2432-2435.2001
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
2001
detail.hit.zdb_id:
1496156-8
SSG:
12
SSG:
15,3
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