Yeast protective response to arsenate involves the repression of the high affinity iron uptake system.


Journal Article

Arsenic is a double-edge sword. On the one hand it is powerful carcinogen and on the other it is used therapeutically to treat acute promyelocytic leukemia. Here we report that arsenic activates the iron responsive transcription factor, Aft1, as a consequence of a defective high-affinity iron uptake mediated by Fet3 and Ftr1, whose mRNAs are drastically decreased upon arsenic exposure. Moreover, arsenic causes the internalization and degradation of Fet3. Most importantly, fet3ftr1 mutant exhibits increased arsenic resistance and decreased arsenic accumulation over the wild-type suggesting that Fet3 plays a role in arsenic toxicity. Finally we provide data suggesting that arsenic also disrupts iron uptake in mammals and the link between Fet3, arsenic and iron, can be relevant to clinical applications.

Full Text

Duke Authors

Cited Authors

  • Batista-Nascimento, L; Toledano, MB; Thiele, DJ; Rodrigues-Pousada, C

Published Date

  • May 2013

Published In

Volume / Issue

  • 1833 / 5

Start / End Page

  • 997 - 1005

PubMed ID

  • 23295455

Pubmed Central ID

  • 23295455

International Standard Serial Number (ISSN)

  • 0006-3002

Digital Object Identifier (DOI)

  • 10.1016/j.bbamcr.2012.12.018


  • eng

Conference Location

  • Netherlands