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

Claudina Amélia Pousada

doi:10.1016/j.bbamcr.2012.12.018

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

Claudina Amélia Pousada

Instituto de Tecnologia Química e Biológica António Xavier (ITQB)

Research output: Contribution to journal › Article › peer-review

16 Citations (Scopus)

Abstract

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. (C) 2013 Elsevier B.V. All rights reserved.

Original language	Unknown
Pages (from-to)	997-1005
Journal	Biochimica Et Biophysica Acta-Molecular Cell Research
Volume	1833
Issue number	5
DOIs	https://doi.org/10.1016/j.bbamcr.2012.12.018
Publication status	Published - 1 Jan 2013

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10.1016/j.bbamcr.2012.12.018

Cite this

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title = "Yeast protective response to arsenate involves the repression of the high affinity iron uptake system",

abstract = "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. (C) 2013 Elsevier B.V. All rights reserved.",

keywords = "Iron deficiency, Arsenic uptake, Fet3-Ftr1",

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AU - Pousada, Claudina Amélia

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AB - 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. (C) 2013 Elsevier B.V. All rights reserved.

KW - Iron deficiency

KW - Arsenic uptake

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U2 - 10.1016/j.bbamcr.2012.12.018

DO - 10.1016/j.bbamcr.2012.12.018

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