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\title{Identification of novel arsenic resistance genes in yeast}



\author[1]{Esin Isik}%
\author[1]{Çiğdem Balkan}%
\author[2]{Vivien Karl}%
\author[1]{Hüseyin Çağlar Karakaya}%
\author[2]{Sansan Hua}%
\author[3]{Sebastien Rauch}%
\author[2]{Markus Tamas}%
\author[1]{Ahmet Koc}%
\affil[1]{Izmir Institute of Technology}%
\affil[2]{University of Gothenburg}%
\affil[3]{Chalmers University of Technology}%


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  \date{May 23, 2024}


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\begin{abstract}
Arsenic is a toxic metalloid that affects human health by causing
numerous diseases and by being used in the treatment of acute
promyelocytic leukemia. Saccharomyces cerevisiae (budding yeast) has
been extensively utilized to elucidate the molecular mechanisms
underlying arsenic toxicity and resistance in eukaryotes. In this study,
we applied a genomic DNA overexpression strategy to identify yeast genes
that provide arsenic resistance in wild-type and arsenic-sensitive S.
cerevisiae cells. In addition to known arsenic-related genes, our
genetic screen revealed novel genes, including PHO86, VBA3, UGP1, and
TUL1, whose overexpression conferred resistance. To gain insights into
possible resistance mechanisms, we addressed the contribution of these
genes to cell growth, intracellular arsenic, and protein aggregation
during arsenate exposure. Overexpression of PHO86 resulted in higher
cellular arsenic levels but no additional effect on protein aggregation,
indicating that these cells efficiently protect their intracellular
environment. VBA3 overexpression caused resistance despite higher
intracellular arsenic and protein aggregation levels. Overexpression of
UGP1 led to lower intracellular arsenic and protein aggregation levels
whilst TUL1 overexpression had no impact on intracellular arsenic or
protein aggregation levels. Thus, the identified genes appear to confer
arsenic resistance through distinct mechanisms but the molecular details
remain to be elucidated.%
\end{abstract}%



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