Iron, a major protein cofactor, is essential for most organisms but can be toxic simultaneously. Iron homeostasis thus has to be effectively maintained under a range of iron regimes. This may be particularly true with , a representative of dissimilatory metal-reducing bacteria (DMRB) capable of respiring a variety of chemicals as electron acceptors (EAs), including iron ores. Although iron respiration and its regulation have been extensively studied in this bacterium, how iron homeostasis is maintained remains largely unknown. Here, we report that the loss of iron homeostasis master regulator Fur negatively affects respiration of all EAs tested. This defect appears mainly to be a result of reduced cytochrome (cyt ) production, despite a decrease in expression of reductases that are under the direct control of Fur. We also show that Fur interacts with canonical Fur-box motifs in F-F-x-R configuration rather than the palindromic motif proposed before. The mutant has lowered total iron and increased free iron contents. Under iron-rich conditions overproduction of major iron storage protein Bfr elevates total iron levels of the mutant over that of the wild-type but does not affect free iron levels. Intriguingly, such an operation only marginally improves cyt production through affecting heme biosynthesis. It is established that iron dictates heme /cyt biosynthesis in strains, but the mutation annuls the dependence of heme /cyt biosynthesis on iron. Overall, our results suggest that Fur has a profound impact on iron homeostasis of , through which many physiological processes, especially respiration, are transformed. Iron reduction is a signature of and this process relies on a large number of cyts, which are iron-containing proteins. Thus, iron plays an essential and special role in iron respiration, but to date the iron metabolism and regulation of the bacterium remains largely unknown. In this study, we investigated impacts of Fur, the master regulator of iron homeostasis, on respiration. The loss of Fur causes a general defect in respiration, a result of impaired cyt production rather than specific regulation. Additionally, the mutant is unresponsive to iron, resulting in imbalanced iron homeostasis and dissociation between iron and cyt production. These findings provide important insights into the iron biology of DMRB.
Shewanella oneidensis is among the first and the best studied bacteria capable of respiring minerals as terminal electron acceptors (EAs), including a variety of iron ores. This respiration process relies on a large number of c-type cytochromes, which per se are iron-containing proteins. Thus, iron plays an essential and special role in iron respiration of S. oneidensis, prompting extensive investigations into iron physiology. Despite this, we still know surprisingly little about the components and characteristics of iron transport in this bacterium. Here, we report that TonB-dependent receptor PutA (SO_3033) is specific to the siderophore-mediated iron uptake. Although homologs of PutA are abundant, none of them can function as a replacement. In the absence of PutA, S. oneidensis suffers from an iron shortage, which leads to a severe defect in production of cytochrome c. However, proteins requiring other types of cytochromes, such as b and d, do not appear to be significantly impacted. Intriguingly, lactate, but not other carbon sources that are routinely used to support growth, is able to promote iron uptake when PutA is missing. We further show that the lactate-mediated iron import is independent of lactate permeases. Overall, our results suggest that in S. oneidensis the siderophore-dependent pathway plays a key role in iron uptake when iron is limited, but many alternative routes exist.
is an extensively studied bacterium capable of respiring minerals, including a variety of iron ores, as terminal electron acceptors (EAs). Although iron plays an essential and special role in iron respiration of , little has been done to date to investigate the characteristics of iron transport in this bacterium. In this study, we found that all proteins encoded by the cluster for putrebactin ( native siderophore) synthesis (PubABC), recognition-transport of Fe-putrebactin across the outer membrane (PutA), and reduction of ferric putrebactin (PutB) are essential to putrebactin-mediated iron uptake. Although homologs of PutA are many, none can function as its replacement, but some are able to work with other bacterial siderophores. We then showed that Fe-specific Feo is the other primary iron uptake system, based on the synthetical lethal phenotype resulting from the loss of both iron uptake routes. The role of the Feo system in iron uptake appears to be more critical, as growth is significantly impaired by the absence of the system but not of putrebactin. Furthermore, we demonstrate that hydroxyl acids, especially α-types such as lactate, promote iron uptake in a Feo-dependent manner. Overall, our findings underscore the importance of the ferrous iron uptake system in metal-reducing bacteria, providing an insight into iron homeostasis by linking these two biological processes. is among the first- and the best-studied metal-reducing bacteria, with great potential in bioremediation and biotechnology. However, many questions regarding mechanisms closely associated with those applications, such as iron homeostasis, including iron uptake, export, and regulation, remain to be addressed. Here we show that Feo is a primary player in iron uptake in addition to the siderophore-dependent route. The investigation also resolved a few puzzles regarding the unexpected phenotypes of the mutant and lactate-dependent iron uptake. By elucidating the physiological roles of these two important iron uptake systems, this work revealed the breadth of the impacts of iron uptake systems on the biological processes.
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