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Z4.09 - Electrochemical Mechanisms of Accelerated Anodic Respiration by Shewanella Oneidensis MR-1 Chemically Modified with Membrane-Intercalating Conjugated Oligoelectrolytes 
Date/Time:
April 23, 2014   11:30am - 11:45am
 
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Shewanella oneidensis MR-1 is a well-characterized dissimilatory metal-reducing bacterium that has burgeoned as a model exoelectrogenic species in the last decade. Appropriately poised graphite electrodes may serve as electrochemical electron accepting proxies for MR-1's native respiratory substrates (such as ferric iron minerals), and this has allowed for excellent electrochemical characterization of the species in 3-electrode type reactors. In particular, many studies have explored the mechanistic roles and interplay of the Mtr (metal reduction) electron transport pathway and the biosynthesized flavin electron shuttles that are characteristic to MR-1. From these studies, it is now well understood that MR-1 respires (i.e. donates electrons) in anaerobic environments by utilizing a combination of both direct electron transfer (DET) through cytochromes of the Mtr pathway and mediated electron transfer (MET) via redox cycling of flavin molecules between the bacterium and the acceptor surface. Recently, a growing body of literature has suggested that chemical modification of various microorganisms with micromolar concentrations of membrane-intercalating conjugated oligoelectrolytes (COEs) will accelerate extracellular electron transport (EET) from the organisms to an electrode acceptor. The universal observation of such EET acceleration would seem to be analogous to the natural EET observed in MR-1, but up to this point, a straightforward mechanistic picture of the accelerated EET afforded by COEs has remained elusive. From a technology-development standpoint, it is extremely important to understand this acceleration mechanism and whether DET or MET processes are involved. MR-1 undergoes both types of EET and thus serves as an excellent model organism for exploring exactly this COE-EET mechanism. This presentation will outline the 3-electrode amperometry and voltammetry, as well as electron microscopy and other experiments, which suggest that COEs increase anodic respiration of MR-1 via DET by activating a subdued electrochemical pathway (non-flavin, non-cytochrome, but still biological) without significant cytotoxicity. These results may have strong implications for understanding the effect of COEs on other species in bioelectrochemical systems.
 


 
 
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