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A Novel Approach to the Discovery of Natural Products From Actinobacteria

Actinobacteria, primarily the genus Streptomyces, have led to the development of a number of antibiotics, which result from their secondary metabolites or modified derivatives. Secondary metabolite production can result from competition with neighboring microbes in an effort to disrupt growth, aiding in the competition for vital nutrients in impoverished conditions. Such secondary metabolites have the potential to affect a plethora of cellular functions in target cells, including, cell wall development, protein synthesis, protein function and fatty acid synthesis/metabolism. Due to the pandemic spread of antibiotic resistant bacteria, it is imperative to continue the search for new therapeutic agents targeting these deadly organisms. As such, our group explored soil and marine samples from Tampa Bay’s surrounding farmlands and waterways for secondary metabolite producing microbes using culture methods specific to Actinobacteria. Through these efforts we isolated over 750 bacterial species, of which almost half are confirmed Actinobacteria. In an attempt to derive new and novel chemistry from these organisms, we used our novel collection, and developed techniques for epigenetic modification to un-silence dormant and cryptic metabolic pathways. Our work reveals that a number of these Actinobacteria produce secondary metabolites that are effective against the ESKAPE pathogens, some at very low concentrations. Although the bioactivity from secondary metabolites is a well-known source for antibiotic drug discovery, our epigenetic methods suggest a potential to isolate previously overlooked compounds that have a very real possibility for use as antibacterial therapeutics.

Identiferoai:union.ndltd.org:USF/oai:scholarcommons.usf.edu:etd-7963
Date24 March 2017
CreatorsTawfik, Rahmy
PublisherScholar Commons
Source SetsUniversity of South Flordia
Detected LanguageEnglish
Typetext
Formatapplication/pdf
SourceGraduate Theses and Dissertations
Rightsdefault

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