Transcriptional regulation of Fe–S biogenesis genes: A possible shield against arsenate toxicity activated by Yap1

Sofia M. da Silva, Liliana Batista-Nascimento, Ana Gaspar-Cordeiro, Laurence Vernis, Catarina Pimentel, Claudina Rodrigues-Pousada

Research output: Contribution to journalArticlepeer-review

2 Citations (Scopus)

Abstract

In the eukaryotic model yeast Saccharomyces cerevisiae, arsenic (As) detoxification is regulated by two transcriptional factors, Yap8 and Yap1. Yap8 specifically controls As extrusion from the cell, whether Yap1 avoids arsenic-induced oxidative damages. Accordingly, cells lacking both Yap1 and Yap8 are more sensitive to arsenate than cells lacking each regulator individually. Strikingly enough, the same sensitivity pattern was observed under anoxia, suggesting that Yap1 role in As detoxification might not be restricted to the regulation of the oxidative stress response. This finding prompted us to study the transcriptomic profile of wild-type and yap1 mutant cells exposed to arsenate. Interestingly, we found that, under such conditions, several genes involved in the biogenesis of Fe–S proteins were upregulated in a Yap1-dependent way. In line with this observation, arsenate treatment decreases the activity of the mitochondrial aconitase, Aco1, an Fe–S cluster-containing enzyme, this effect being even more pronounced in the yap1 mutant. Reinforcing the relevance of Fe–S cluster biogenesis in arsenate detoxification, the overexpression of several ISC and CIA machinery genes alleviates the deleterious effect of arsenate caused by the absence of Yap1 and Yap8. Altogether our data suggest that the upregulation of Fe–S biogenesis genes regulated by Yap1 might work as a cellular shield against arsenate toxicity.

Original languageEnglish
Pages (from-to)2152-2161
Number of pages10
JournalBiochimica et Biophysica Acta - General Subjects
Volume1862
Issue number10
DOIs
Publication statusPublished - 1 Oct 2018

Keywords

  • Arsenate
  • Fe–S biogenesis
  • Iron homeostasis
  • Stress
  • Yap1

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