To further demonstrate the functional role of UndA in iron reduction, competition assays were carried out to examine the fitness

gain/loss caused by undA deletion. When wild-type and ∆undA cells were co-cultured in a medium with ferric citrate as the electron acceptor (Figure 4A), wild-type outcompeted ∆undA and gradually became dominant in the population by daily transfers. Similarly, ΔmtrC outcompeted ΔmtrC-undA (Figure 4B). These results indicated that UndA was needed BAY 73-4506 mouse to provide fitness advantage under iron-reducing conditions. Figure 4 The competition Assay for (A) wild-type (WT) vs. Δ undA and (B) Δ mtrC vs. Δ mtrC-undA . Relative abundances of each strain in the co-culture at Day 1, 3 and 7 are shown. Discussion Shewanella are

commonly present in redox stratified environments [13]. The successful establishment in such niches requires that bacteria adapt to utilize the electron donor or acceptor types in the environment. Accordingly, Shewanella strains are remarkable in utilizing a wide range of electron acceptors. Recent studies showed that S. putrefaciens W3-18-1 exhibited strong reduction of hydrous ferric oxide [30] as well as growth with DNA as sole carbon and energy source [31]. In addition, it could reduce metals and form magnetite at 0°C [15]. GSK1210151A solubility dmso Here we further demonstrated that S. putrefaciens W3-18-1 was potent in reducing α-FeO(OH), ferric citrate, β-FeO(OH) and Fe2O3, which might be linked to the iron reduction gene cluster of W3-18-1. Notably, this gene cluster differs substantially from that of MR-1 in that it is comprised of only four genes (mtrBAC and undA) (Figure 2A). The mutational analysis in our study indicated that MtrC was {Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|Selleck Anti-diabetic Compound Library|Selleck Antidiabetic Compound Library|Selleckchem Anti-diabetic Compound Library|Selleckchem Antidiabetic Compound Library|Selleckchem Anti-diabetic Compound Library|Selleckchem Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|Anti-diabetic Compound Library|Antidiabetic Compound Library|buy Anti-diabetic Compound Library|Anti-diabetic Compound Library ic50|Anti-diabetic Compound Library price|Anti-diabetic Compound Library cost|Anti-diabetic Compound Library solubility dmso|Anti-diabetic Compound Library purchase|Anti-diabetic Compound Library manufacturer|Anti-diabetic Compound Library research buy|Anti-diabetic Compound Library order|Anti-diabetic Compound Library mouse|Anti-diabetic Compound Library chemical structure|Anti-diabetic Compound Library mw|Anti-diabetic Compound Library molecular weight|Anti-diabetic Compound Library datasheet|Anti-diabetic Compound Library supplier|Anti-diabetic Compound Library in vitro|Anti-diabetic Compound Library cell line|Anti-diabetic Compound Library concentration|Anti-diabetic Compound Library nmr|Anti-diabetic Compound Library in vivo|Anti-diabetic Compound Library clinical trial|Anti-diabetic Compound Library cell assay|Anti-diabetic Compound Library screening|Anti-diabetic Compound Library high throughput|buy Antidiabetic Compound Library|Antidiabetic Compound Library ic50|Antidiabetic Compound Library price|Antidiabetic Compound Library cost|Antidiabetic Compound Library solubility dmso|Antidiabetic Compound Library purchase|Antidiabetic Compound Library manufacturer|Antidiabetic Compound Library research buy|Antidiabetic Compound Library order|Antidiabetic Compound Library chemical structure|Antidiabetic Compound Library datasheet|Antidiabetic Compound Library supplier|Antidiabetic Compound Library in vitro|Antidiabetic Compound Library cell line|Antidiabetic Compound Library concentration|Antidiabetic Compound Library clinical trial|Antidiabetic Compound Library cell assay|Antidiabetic Compound Library screening|Antidiabetic Compound Library high throughput|Anti-diabetic Compound high throughput screening| specifically important for metal reduction (Figure 3 & Additional file 1: Figure S2), which was consistent with previous reports that its orthologs

Diflunisal in other Shewanella strains played an important role in iron reduction [11, 12]. In contrast, UndA was involved in, but not required for iron reduction. Based on these data, it appears that MtrC and UndA are primary and auxiliary components of iron reduction pathways, respectively. Recent success in resolving the crystal structure of Shewanella sp. strain HRCR-6 UndA has revealed binding sites for soluble iron chelators [32]. Consistently, our iron reduction and competition experiments suggested that UndA was indeed involved in iron reduction. As a predicted outer membrane lipoprotein, S. putrefaciens UndA might directly interact with extracellular metals. A recent study showed that the UndA ortholog in Shewanella sp. strain HRCR-6 was secreted extracellularly by type II secretion system and participated in ferrihydrite and U(VI) reduction [33]. Interestingly, overexpressing UndA of HRCR-6 partially restored the iron reduction deficiency of ΔmtrC-omcA mutant. It is likely that overexpressing S.