7%), most of which lack homologs in G. sulfurreducens and this website may be recent acquisitions (Additional file 1: Table S1). Clusters of such genes (shaded in Additional file 1: Table S1) were often interrupted or flanked by transposons with higher G+C content. The functions of most of these genes cannot be assigned at present, but 23 of them are predicted to act in cell wall biogenesis. Plasmid pMET1 of G. metallireducens consists of a series of six
predicted transcriptional units on one strand, tentatively attributed to the mobilization (Gmet_A3575-Gmet_A3574-Gmet_A3573-Gmet_A3572-Gmet_A3643), entry exclusion (Gmet_A3571), addiction (Gmet_A3570-Gmet_A3579-Gmet_A3642), partition (Gmet_A3568-Gmet_A3641), transposition (Gmet_A3567), and replication (Gmet_A3566-Gmet_A3565) functions of the plasmid, and one operon on the opposite strand, comprised
of three genes of unknown function (Gmet_A3576-Gmet_A3577-Gmet_A3644). The predicted origin of replication, located 3′ of the repA gene (Gmet_A3565), includes four pairs of iterons and a set of six hairpins, suggesting that pMET1 replicates by a rolling-circle mechanism, although it is significantly larger than most such plasmids [13]. Among the PU-H71 order fifteen other nucleotide sequence features identified on the plasmid during manual curation was a palindromic putative autoregulatory site (TTTGTTATACACGTATAACAAA) located 5′ of the addiction module. Other than the potential toxicity of the addiction module, the impact of pMET1 on the physiology
of G. metallireducens is unknown. Metabolism of acetate and other carbon sources Acetate is expected to be the key electron donor supporting Fe(III) reduction in aquatic sediments and subsurface environments [14], and Geobacter species quickly become the predominant bacterial species when acetate is injected into subsurface environments to promote in situ bioremedation of uranium-contaminated groundwater [15, 16]. Surprisingly, the initial activation of acetate by ligation with coenzyme A (CoA) in G. sulfurreducens selleck inhibitor occurs by two reversible Etomidate pathways [17] (Figure 1), indicating that acetate may be inefficiently utilized at low concentrations. These two pathways are also present in G. metallireducens, along with a third, irreversible reaction that may permit efficient activation of acetate at low concentrations. The first pathway of acetate activation (Figure 1a) occurs through either of two succinyl:acetate CoA-transferases that can convert succinyl-CoA to succinate during oxidation of acetate by the tricarboxylic acid (TCA) cycle pathway, in the same capacity as succinyl-CoA synthetase but conserving energy in the form of acetyl-CoA rather than GTP or ATP [17].