ArticlePloS one2018
The Ferric uptake regulator (Fur) and iron availability control the production and maturation of the antibacterial peptide microcin E492.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 17 citations in OpenAlex.
- A Non-genotoxic Variant of Escherichia coli Nissle 1917 EcN 2.0 Overexpressing Microcins Reduces Intestinal Carriage of ST131 ESBL-Producing Escherichia coli.Probiotics and antimicrobial proteins · 2026Article
- The C-terminal domain of the ferric uptake regulator (Fur) binds a [2Fe-2S] cluster to sense the intracellular free iron content in Escherichia coli.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023Article
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- Ferric uptake regulator (Fur) binds a [2Fe-2S] cluster to regulate intracellular iron homeostasis in Escherichia coli.The Journal of biological chemistry · 2023Article
- Mcc1229, an Stx2a-Amplifying Microcin, Is ProducedInfection and immunity · 2022Article
- Manganese Privation-Induced Transcriptional Upregulation of the Class IIa Bacteriocin Plantaricin 423 in Lactobacillus plantarum Strain 423.Applied and environmental microbiology · 2021Article
- An unusual overrepresentation of genetic factors related to iron homeostasis in the genome of the fluorescent Pseudomonas sp. ABC1.Microbial biotechnology · 2021Article
- SynBio and the Boundaries between Functional and Pathogenic RepA-WH1 Bacterial Amyloids.mSystems · 2020Review
- Siderophore-Microcins inFrontiers in cellular and infection microbiology · 2020Review
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7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Microcin E492 is a pore-forming bacteriocin with toxic activity against Enterobacteriaceae, which undergoes amyloid aggregation as a mechanism to regulate its toxicity. To be active, it requires the posttranslational attachment to the C-terminus of a glycosylated enterochelin derivative (salmochelin), a process carried out by the proteins MceC, MceI and MceJ encoded in the MccE492 gene cluster. Both microcin E492 and salmochelin have a proposed role in the virulence of the bacterial pathogen Klebsiella pneumoniae. Besides, enterochelin is produced as a response to low iron availability and its synthesis is controlled by the global iron regulator Fur. Since the production of active microcin E492 depends on enterochelin biosynthesis, both processes could be coordinately regulated. In this work, we investigated the role of Fur in the expression of the microcin E492 maturation genes mceCJI. mceC was not regulated by Fur as it occurs with its homolog iroB in Salmonella enterica. We demonstrated that mceJI along with the previously uncharacterized gene mceX are transcribed as a single mRNA, and that Fur binds in vivo to a Fur box located upstream of the mceX-mceJI unit. Also, we established that the expression of these genes decreased in a condition of high iron availability, while this effect is abrogated in a Δfur background. Furthermore, our results indicated that MceX acts as a negative regulator of microcin E492 structural gene expression, coupling its synthesis to the iron-dependent regulatory circuit. Consequently, fur or mceX overexpression led to a significant decrease in the antibacterial activity of cells producing microcin E492. Altogether these results show that both the expression of microcin E492 maturation genes mceJI, and MceX the negative regulator of microcin E492 synthesis, are coordinated with the enterochelin production by Fur, depending on the iron levels in the medium.
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