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Calcium signaling and copper toxicity in Saccharomyces cerevisiae cells

  • Global pollution problems, Trends in Detection and Protection
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Abstract

To respond to metal surpluses, cells have developed intricate ways of defense against the excessive metallic ions. To understand the ways in which cells sense the presence of toxic concentration in the environment, the role of Ca2+ in mediating the cell response to high Cu2+ was investigated in Saccharomyces cerevisiae cells. It was found that the cell exposure to high Cu2+ was accompanied by elevations in cytosolic Ca2+ with patterns that were influenced not only by Cu2+ concentration but also by the oxidative state of the cell. When Ca2+ channel deletion mutants were used, it was revealed that the main contributor to the cytosolic Ca2+ pool under Cu2+ stress was the vacuolar Ca2+ channel, Yvc1, also activated by the Cch1-mediated Ca2+ influx. Using yeast mutants defective in the Cu2+ transport across the plasma membrane, it was found that the Cu2+-dependent Ca2+ elevation could correlate not only with the accumulated metal, but also with the overall oxidative status. Moreover, it was revealed that Cu2+ and H2O2 acted in synergy to induce Ca2+-mediated responses to external stress.

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Acknowledgments

We thank Prof. Enzo Martegani and Dr. Renata Tisi (from University of Milano-Bicocca, Milan, Italy) for providing the plasmid pYX212-cytAEQ and Prof. Andrei F. Danet for technical support. The research leading to these results has received funding from the Romanian–EEA Research Programme operated by the Ministry of National Education under the EEA Financial Mechanism 2009–2014 and Project Contract No 21 SEE/30.06.2014 and by the Executive Unit for Higher Education, Development, Research and Innovation Funding–UEFISCDI, Romania, under Grant PN-II-PT-PCCA-2013-4-0291 (contract no. 203/2014).

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Correspondence to Ileana C. Farcasanu.

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Ruta, L.L., Popa, C.V., Nicolau, I. et al. Calcium signaling and copper toxicity in Saccharomyces cerevisiae cells. Environ Sci Pollut Res 23, 24514–24526 (2016). https://doi.org/10.1007/s11356-016-6666-5

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  • DOI: https://doi.org/10.1007/s11356-016-6666-5

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