Get access

Molecular biology of iron acquisition in Saccharomyces cerevisiae

Authors

  • Candice C. Askwith,

    1. Division of immunology and Cell Biology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
    Search for more papers by this author
  • Deepika de Silva,

    1. Division of immunology and Cell Biology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
    Search for more papers by this author
  • Jerry Kaplan

    Corresponding author
    1. Division of immunology and Cell Biology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, Utah 84132, USA.
    • *For correspondence. Tel. (801) 581 7427; Fax (801)581 4517.

    Search for more papers by this author

Summary

In recent years, significant advances have been made in our understanding of the mechanism and regulation of elemental iron transport in the eukaryote Saccharomyces cerevisiae. This organism employs two distinct iron-transport systems, depending on the bioavailability of the metal. In iron-replete environments, a low-affinity transport system (Km=30μM) is used to acquire iron. This system may also be used to acquire other metals including cobalt and cadmium. When environmental iron is limiting, a high-affinity (Km=0.15 μM) iron-transport system is induced. Genetic studies in S. cerevisiae have identified multiple genes involved in both iron-transport systems. Cell-surface reductases, FRE1 and FRE2, provide ferrous iron for both systems. A non-ATP-dependent transmembrane transporter (FET4) has been identified as the main component of low-affinity transport. One gene identified to date as part of the high-affinity transport system is FET3, which shows high sequence and functional homology to multicopper oxidases. Accessory genes required for the functioning of this transport system include a plasma-membrane copper transporter (CTR1), an intracellular copper transporter (CCC2), and a putative transcription factor (AFT1). The mechanism by which these genes act in concert to ensure iron accumulation in S. cerevisiae presents an intriguing picture, drawing parallels with observations made in the human system almost 40 years ago.

Get access to the full text of this article

Ancillary