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Transcriptomic response of Enterococcus faecalis to iron excess.

Guadalupe López1, Mauricio Latorre, Angélica Reyes-Jara

  • 1Laboratorio de Bioinformática y Expresión Génica, INTA, Universidad de Chile, El Líbano 5524, Macul, Santiago, Chile. glopez@inta.uchile.cl

Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine
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Summary

Enterococcus faecalis activates adaptive gene expression to maintain iron homeostasis during iron excess. This response involves regulating specific transporters and stress proteins, with some overlap with oxidative stress responses.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Physiology

Background:

  • Iron is crucial for bacterial growth, yet molecular mechanisms of iron homeostasis are not fully understood.
  • Enterococcus faecalis regulates gene expression in response to varying iron availability to maintain cellular balance.

Purpose of the Study:

  • To identify genes in Enterococcus faecalis that respond to increased intracellular iron levels.
  • To elucidate the transcriptional mechanisms underlying iron homeostasis in E. faecalis.

Main Methods:

  • Global transcriptional analysis (transcriptomics) of E. faecalis under non-toxic iron excess.
  • Gene expression analysis following treatment with hydrogen peroxide (H2O2) and the iron chelator 2,2-dipyridyl.
  • Comparison of transcriptomic data with previously published gene expression data from E. faecalis grown in blood.

Main Results:

  • Up-regulation of Fur family regulators (PerR, ZurR), cation efflux (CzcD), and ferredoxin.
  • Down-regulation of MntH transporters and UspA under iron excess.
  • Partial overlap between iron-induced and oxidative stress-induced transcriptional changes; iron uptake genes (feo, ycl) upregulated in blood, suggesting iron-deficient conditions.

Conclusions:

  • E. faecalis employs an adaptive transcriptional response to manage iron excess and maintain homeostasis.
  • Oxidative stress partially mediates iron-induced transcriptional changes.
  • Blood culture conditions mimic iron deficiency for E. faecalis, activating iron uptake systems.