Abstract

Iron (Fe) is a double-edged sword for most living organisms. Although it is essential for the catalytic activity of a large number of enzymes, ferrous iron (Fe(2+) ) becomes cytotoxic in the presence of normal respiratory by-products such as H(2) O(2) . Because of this toxicity, intracellular iron concentrations ought to be regulated by elaborated homeostasis systems that, despite decades of extensive studies, have not yet revealed all of their surprising arrays of mechanistic details. Within the last few years, our understanding of iron metabolism has revealed that posttranscriptional regulation represents a major contribution to iron homeostasis in a host of organisms. While the small RNA RyhB regulates iron homeostasis in bacteria, its functional homolog protein Cth2 performs a similar task in yeasts. Recent advances in the elucidation of the mechanism of action and functions of RyhB have been made in Escherichia coli. In addition, other RyhB-like small RNAs have been identified in several bacterial species, such as Pseudomonas aeruginosa, Salmonella enterica, Vibrio cholerae, Neisseria meningitidis, and Shigella spp. These recent findings have shed light on the complexity of iron homeostasis.

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