Journal
BIOMETALS
Volume 25, Issue 4, Pages 737-747Publisher
SPRINGER
DOI: 10.1007/s10534-012-9539-5
Keywords
Enteroccocus faecalis; Iron transporters; Global gene expression; qPCR; Iron content; Oxidative stress
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Funding
- Fondo Nacional de Desarrollo Cientifico y Tecnologico, FONDECYT [1110427, 1090211]
- Fondo Nacional de Desarrollo de Areas Prioritarias, FONDAP, Center for Genome Regulation (CGR) [15090007]
- Insercion de Capital Humano Avanzado en la Academia from CONICYT [791100002]
- CONICYT
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Iron is an essential nutrient for sustaining bacterial growth; however, little is known about the molecular mechanisms that govern gene expression during the homeostatic response to iron availability. In this study we analyzed the global transcriptional response of Enterococcus faecalis to a non-toxic iron excess in order to identify the set of genes that respond to an increment of intracellular iron. Our results showed an up-regulation of transcriptional regulators of the Fur family (PerR and ZurR), the cation efflux family (CzcD) and ferredoxin, while proton-dependent Mn/Fe (MntH) transporters and the universal stress protein (UspA) were down-regulated. This indicated that E. faecalis was able to activate a transcriptional response while growing in the presence of an excess of non-toxic iron, assuring the maintenance of iron homeostasis. Gene expression analysis of E. faecalis treated with H2O2 indicated that a fraction of the transcriptional changes induced by iron appears to be mediated by oxidative stress. A comparison of our transcriptomic data with a recently reported set of differentially expressed genes in E. faecalis grown in blood, revealed an important fraction of common genes. In particular, genes associated to oxidative stress were up-regulated in both conditions, while genes encoding the iron uptake system (feo and ycl operons) were up-regulated when cells were grown in blood. This suggested that blood cultures mimic an iron deficit, and was corroborated by measuring feo and ycl expression in E. faecalis treated with the iron chelating agent 2,2-dipyridil. In summary, our group identified an adaptive transcriptional mechanism in response to metal ion stress in E. faecalis, providing a foundation for future in-depth functional studies of the iron-activated regulatory network.
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