Abstract
BackgroundIt is well established in E. coli and Vibrio cholerae that strains harboring mutations in the ferric uptake regulator gene (fur) are unable to utilize tricarboxylic acid (TCA) compounds, due to the down-regulation of key TCA cycle enzymes, such as AcnA and SdhABCD. This down-regulation is mediated by a Fur-regulated small regulatory RNA named RyhB. It is unclear in the γ-proteobacterium S. oneidensis whether TCA is also regulated by Fur and RyhB.ResultsIn the present study, we showed that a fur deletion mutant of S. oneidensis could utilize TCA compounds. Consistently, expression of the TCA cycle genes acnA and sdhA was not down-regulated in the mutant. To explore this observation further, we identified a ryhB gene in Shewanella species and experimentally demonstrated the gene expression. Further experiments suggested that RyhB was up-regulated in fur mutant, but that AcnA and SdhA were not controlled by RyhB.ConclusionsThese cumulative results delineate an important difference of the Fur-RyhB regulatory cycle between S. oneidensis and other γ-proteobacteria. This work represents a step forward for understanding the unique regulation in S. oneidensis.
Highlights
It is well established in E. coli and Vibrio cholerae that strains harboring mutations in the ferric uptake regulator gene are unable to utilize tricarboxylic acid (TCA) compounds, due to the down-regulation of key TCA cycle enzymes, such as AcnA and SdhABCD
TCA cycle activity and regulation in the fur mutant We showed recently that S. oneidensis harboring a fur deletion in the genome was sensitive to acidic conditions and de-repressed genes encoding iron acquisition systems [11]
The involvement of Fur in this biological process has been established in E. coli and V. cholerae by observations that fur mutants are unable to grow in defined media with succinate or fumarate as a carbon source [9,16], and that genes encoding certain TCA cycle enzymes, such as succinate dehydrogenase (SdhABCD) and aconitase (AcnA), are significantly down-regulated in a fur mutant [7]
Summary
It is well established in E. coli and Vibrio cholerae that strains harboring mutations in the ferric uptake regulator gene (fur) are unable to utilize tricarboxylic acid (TCA) compounds, due to the down-regulation of key TCA cycle enzymes, such as AcnA and SdhABCD. This down-regulation is mediated by a Fur-regulated small regulatory RNA named RyhB. Physiological, transcriptomics and proteomics studies have shown that S. oneidensis Fur regulates genes involved in iron homeostasis and acid resistance [10,11,12,13] Many of these target genes have a recognizable “Fur box” in their promoters. These results delineate differences in the gene regulation and physiological consequences of RyhB between S. oneidensis and E. coli
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