The Saccharomyces cerevisiae response to stress caused by the herbicidal active substance alachlor requires the iron regulon transcription factor Aft1p.

Abstract

In the Saccharomyces cerevisiae eukaryotic model, the induction of the iron regulon genes ARN1, FIT2 and CTH2 by growth-inhibitory concentrations of alachlor (ALA) was dependent on Aft1p expression. This transcription factor was found to be activated through its nuclear localization. The hypersensitivity of the aft1Δ mutant to ALA was abrogated by surplus exogenous iron, suggesting that the role of Aft1p in ALA tolerance may be associated with iron limitation under ALA stress. A transient decrease in the cellular iron content in the ALA-stressed cells supported this idea. In contrast to the upregulation of the nonreductive iron uptake genes ARN1 and FIT2 by ALA, thequantity of FET3 and FTR1 transcripts encoding the high-affinity iron uptake reductive pathway decreased. Yeast cells were apparently more sensitive to ALA when iron uptake occurred through the reductive pathway than when the nonreductive uptake of ferrichrome-bound ferric iron was dominant. On the other hand, the ALA hypersensitivity of the aft1Δ mutant was reversed by medium supplementation with glutathione or N-acetyl-L-cysteine. The results are compatible with possible links between ALA toxicity and perturbations in metal and antioxidant homeostasis, which may be relevant for environmental microbes and higher eukaryotes in situations of inadvertent herbicide contamination.