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- W2121506548 abstract "Abstract Ypi1 was discovered as an essential protein able to act as a regulatory subunit of the Saccharomyces cerevisiae type 1 protein phosphatase Glc7 and play a key role in mitosis. We show here that partial depletion of Ypi1 causes lithium sensitivity and that high levels of this protein confer a lithium-tolerant phenotype to yeast cells. Remarkably, this phenotype was independent of the role of Ypi1 as a Glc7 regulatory subunit. Lithium tolerance in cells overexpressing Ypi1 was caused by a combination of increased efflux of lithium, mediated by augmented expression of the alkaline cation ATPase ENA1, and decreased lithium influx through the Trk1,2 high-affinity potassium transporters. Deletion of CNB1, encoding the regulatory subunit of the calcineurin phosphatase, blocked Ypi1-induced expression of ENA1, normalized Li+ fluxes, and abolished the Li+ hypertolerant phenotype of Ypi1-overexpressing cells. These results point to a complex role of Ypi1 on the regulation of cation homeostasis, largely mediated by the calcineurin phosphatase." @default.
- W2121506548 created "2016-06-24" @default.
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- W2121506548 date "2012-04-01" @default.
- W2121506548 modified "2023-10-16" @default.
- W2121506548 title "Modulation of Yeast Alkaline Cation Tolerance by Ypi1 Requires Calcineurin" @default.
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- W2121506548 doi "https://doi.org/10.1534/genetics.112.138370" @default.
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