Electrochemical investigations into Electrode directed Taxis and Extracellular Electron Transfer Mechanisms of Shewanella oneidensis MR-1

Shewanella oneidensis MR-1 is capable of respiring on an extraordinarily large and diverse array of terminal electron acceptors, including extracellular insoluble metal oxides and electrodes. The ability to perform extracellular electron transfer (EET) has sparked great interest in MR-1 which has become both a model organism for fundamental research into EET and a candidate microbe for microbial electrochemical systems. Here, cyclic voltammetry was used to determine the relationship between the surface chemistry of electrodes (modified gold, ITO and carbon) and the EET mechanism. On ultra-smooth gold electrodes modified with self-assembled monolayers containing carboxylic acid terminated thiols, an EET pathway dominates with an oxidative onset at 0.1 V (SHE). Addition of the siderophore deferoxamine abolishes this signal, leading us to conclude that this pathway proceeds via an iron mediated electron transfer (MET) mechanism. The same EET pathway is observed on other electrodes but the onset potential is dependent on the electrolyte composition and electrode surface chemistry. EET pathways with onset potentials above -0.1 V (SHE) have previously been ascribed to direct electron transfer (DET) mechanisms via outer membrane cytochromes (MtrC/OmcA). We propose that the previously identified DET mechanisms of MR-1 need to be re-evaluated.
It has been proposed that MR-1 could use flavins for locating insoluble electron acceptors, including electrodes. To assess the role of flavins in MR-1 taxis towards electrodes we performed video microscopy cell tracking using a specifically designed capillary cell and tracking algorithm suited to low frame rates. Analysis of trajectories from WT MR-1 and mutants (ΔmtrC/ΔomcA and Δbfe), showed that MR-1 had a tactic response towards electrodes poised above the midpoint potential of riboflavin (> -0.15 V vs SHE) and a negative response on switching to potentials below the midpoint potential (< -0.25 V vs SHE). The Mtr EET pathway was essential for this response.