Modulation of yeast alkaline cation tolerance by ypi1 requires calcineurin

Maribel Marquina, Asier González, Lina Barreto, Samuel Gelis, Iván Muñoz, Amparo Ruiz, Mari Carmen Álvarez, José Ramos, Joaquín Ariño

Research output: Contribution to journalArticleResearchpeer-review

12 Citations (Scopus)


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. © 2012 by the Genetics Society of America.
Original languageEnglish
Pages (from-to)1355-1364
Issue number4
Publication statusPublished - 1 Apr 2012


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