Platensimycin is a selective FabF inhibitor with potent antibiotic properties - PubMed (original) (raw)
. 2006 May 18;441(7091):358-61.
doi: 10.1038/nature04784.
Stephen M Soisson, Katherine Young, Wesley Shoop, Srinivas Kodali, Andrew Galgoci, Ronald Painter, Gopalakrishnan Parthasarathy, Yui S Tang, Richard Cummings, Sookhee Ha, Karen Dorso, Mary Motyl, Hiranthi Jayasuriya, John Ondeyka, Kithsiri Herath, Chaowei Zhang, Lorraine Hernandez, John Allocco, Angela Basilio, José R Tormo, Olga Genilloud, Francisca Vicente, Fernando Pelaez, Lawrence Colwell, Sang Ho Lee, Bruce Michael, Thomas Felcetto, Charles Gill, Lynn L Silver, Jeffery D Hermes, Ken Bartizal, John Barrett, Dennis Schmatz, Joseph W Becker, Doris Cully, Sheo B Singh
Affiliations
- PMID: 16710421
- DOI: 10.1038/nature04784
Platensimycin is a selective FabF inhibitor with potent antibiotic properties
Jun Wang et al. Nature. 2006.
Abstract
Bacterial infection remains a serious threat to human lives because of emerging resistance to existing antibiotics. Although the scientific community has avidly pursued the discovery of new antibiotics that interact with new targets, these efforts have met with limited success since the early 1960s. Here we report the discovery of platensimycin, a previously unknown class of antibiotics produced by Streptomyces platensis. Platensimycin demonstrates strong, broad-spectrum Gram-positive antibacterial activity by selectively inhibiting cellular lipid biosynthesis. We show that this anti-bacterial effect is exerted through the selective targeting of beta-ketoacyl-(acyl-carrier-protein (ACP)) synthase I/II (FabF/B) in the synthetic pathway of fatty acids. Direct binding assays show that platensimycin interacts specifically with the acyl-enzyme intermediate of the target protein, and X-ray crystallographic studies reveal that a specific conformational change that occurs on acylation must take place before the inhibitor can bind. Treatment with platensimycin eradicates Staphylococcus aureus infection in mice. Because of its unique mode of action, platensimycin shows no cross-resistance to other key antibiotic-resistant strains tested, including methicillin-resistant S. aureus, vancomycin-intermediate S. aureus and vancomycin-resistant enterococci. Platensimycin is the most potent inhibitor reported for the FabF/B condensing enzymes, and is the only inhibitor of these targets that shows broad-spectrum activity, in vivo efficacy and no observed toxicity.
Comment in
- Antibiotic faces uncertain future.
Pearson H. Pearson H. Nature. 2006 May 18;441(7091):260-1. doi: 10.1038/441260a. Nature. 2006. PMID: 16710378 No abstract available. - Microbiology: antibiotic stops 'ping-pong' match.
Brown ED. Brown ED. Nature. 2006 May 18;441(7091):293-4. doi: 10.1038/441293a. Nature. 2006. PMID: 16710404 No abstract available.
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