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How a Microbe Resists its Own Antibiotics

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In the mid-2000s, scientists identified two novel antimicrobial compounds in the bacterium Streptomyces platensis, each of which target a different enzyme involved in fatty acid synthesis in other microbes. Platensimycin and platencin are now being explored as a new class of antibiotics. Research published today (February 20) in Chemistry & Biology from investigators at the University of Wisconsin-Madison and The Scripps Research Institute in Jupiter, Florida, details the mechanism by which S. platensis protects itself from its own antibiotics: the bacterium employs an enzyme during fatty acid synthesis that is unaffected by the compounds.

“It is a nice piece of work and is perhaps one of the first complete demonstrations of antibiotic resistance mechanisms from genome sequencing information,” microbiologist Julian Davies, a professor emeritus at the University of British Columbia who was not involved in the work, told The Scientist in an e-mail.

“The novelty is in the detail here,” agreed David Hopwood, former head of the genetics department and now emeritus fellow at the John Innes Centre, who also did not participate in the research. “It tells us a lot of interesting things about fatty acid biosynthesis in bacteria . . . [and] about the way that the antibiotics interact with [that] pathway.”
 
 

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