A Defense Strategy in Saccharomyces cerevisiae Mediated by the Golgi Chloride Transporter Gef1p to Cope with Nickel Stress
- 1Development Center of Plant Germplasm Resources, College of Life Sciences, Shanghai Normal University, Shanghai 200234, China
- 2Department of Biological Chemistry, University of Michigan, Ann Arbor, MI 48109-0600, USA
Abstract
Nickel is a widespread environmental pollutant originating from industrial activities, and its pollution problem persists globally. Currently, research on nickel ion metabolism and detoxification mechanisms primarily focuses on prokaryotes, while the molecular mechanisms of nickel detoxification in eukaryotes remain underexplored. In this study, Saccharomyces cerevisiae was used as a eukaryotic model to demonstrate that the plasma membrane-localized chloride transporter Gef1p participates in nickel ion metabolism. The GEF1 knockout strain (gef1Δ) showed strong resistance to excess nickel ions, and the content of nickel ions in gef1Δ cells was significantly elevated. The results of transcriptomics analysis showed significant upregulation of MMT2 and CUP1 in gef1Δ cells supplemented with nickel. Both MMT2 and CUP1 overexpressed in the gef1Δ strain showed a growth advantage on nickel media. Nickel ion content in the mitochondria of cells overexpressing MMT2 was significantly elevated, and the levels of reactive oxygen species were significantly decreased in strains overexpressing either the MMT2 or CUP1 genes. This study reveals that the GEF1 gene plays an important role in nickel resistance, and that upregulation of MMT2 and CUP1 is critical for gef1Δ strains to counteract ROS formation and growth defect by nickel ions. The high intracellular accumulation of nickel ions caused by gef1Δ during the process of resisting nickel toxicity makes it a strong candidate for ecological remediation of nickel ion pollution.
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BibTeX
@article{huang2026defense,
title = {{A Defense Strategy in Saccharomyces cerevisiae Mediated by the Golgi Chloride Transporter Gef1p to Cope with Nickel Stress}},
author = {Rongqiu Huang and Xiaoyong Hu and Qianqian Li and Lixuan Zong and Joseph Brake and Chaoyang Luo and Binzhan Wang and Ze Wen and Xiaobin Wu},
journal = {Molecules (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/molecules31193538},
url = {https://europepmc.org/article/PMC/PMC13666631},
note = {CC BY},
}
RIS
TY - JOUR
TI - A Defense Strategy in Saccharomyces cerevisiae Mediated by the Golgi Chloride Transporter Gef1p to Cope with Nickel Stress
AU - Rongqiu Huang
AU - Xiaoyong Hu
AU - Qianqian Li
AU - Lixuan Zong
AU - Joseph Brake
AU - Chaoyang Luo
AU - Binzhan Wang
AU - Ze Wen
AU - Xiaobin Wu
PY - 2026
DA - 2026/10/01
JO - Molecules (Basel, Switzerland)
DO - 10.3390/molecules31193538
UR - https://europepmc.org/article/PMC/PMC13666631
AB - Nickel is a widespread environmental pollutant originating from industrial activities, and its pollution problem persists globally. Currently, research on nickel ion metabolism and detoxification mechanisms primarily focuses on prokaryotes, while the molecular mechanisms of nickel detoxification in eukaryotes remain underexplored. In this study, Saccharomyces cerevisiae was used as a eukaryotic model to demonstrate that the plasma membrane-localized chloride transporter Gef1p participates in nickel ion metabolism. The GEF1 knockout strain (gef1Δ) showed strong resistance to excess nickel ions, and the content of nickel ions in gef1Δ cells was significantly elevated. The results of transcriptomics analysis showed significant upregulation of MMT2 and CUP1 in gef1Δ cells supplemented with nickel. Both MMT2 and CUP1 overexpressed in the gef1Δ strain showed a growth advantage on nickel media. Nickel ion content in the mitochondria of cells overexpressing MMT2 was significantly elevated, and the levels of reactive oxygen species were significantly decreased in strains overexpressing either the MMT2 or CUP1 genes. This study reveals that the GEF1 gene plays an important role in nickel resistance, and that upregulation of MMT2 and CUP1 is critical for gef1Δ strains to counteract ROS formation and growth defect by nickel ions. The high intracellular accumulation of nickel ions caused by gef1Δ during the process of resisting nickel toxicity makes it a strong candidate for ecological remediation of nickel ion pollution.
SN - 1420-3049
ER -