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Eukaryotic Cell, June 2005, p. 1041-1049, Vol. 4, No. 6
1535-9778/05/$08.00+0     doi:10.1128/EC.4.6.1041-1049.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Ability of Sit4p To Promote K⁺ Efflux via Nha1p Is Modulated by Sap155p and Sap185p

Cara Marie A. Manlandro, Devon H. Haydon, and Anne G. Rosenwald^*

Department of Biology, Georgetown University, Washington, D.C. 20057

Received 8 November 2004/ Accepted 21 March 2005

We demonstrate here that SAP155 encodes a negative modulator of K⁺ efflux in the yeast Saccharomyces cerevisiae. Overexpression of SAP155 decreases efflux, whereas deletion increases efflux. In contrast, a homolog of SAP155, called SAP185, encodes a positive modulator of K⁺ efflux: overexpression of SAP185 increases efflux, whereas deletion decreases efflux. Two other homologs, SAP4 and SAP190, are without effect on K⁺ homeostasis. Both SAP155 and SAP185 require the presence of SIT4 for function, which encodes a PP2A-like phosphatase important for the G₁-S transition through the cell cycle. Overexpression of either the outwardly rectifying K⁺ channel, Tok1p, or the putative plasma membrane K⁺/H⁺ antiporter, Kha1p, increases efflux in both wild-type and sit4 strains. However, overexpression of the Na⁺-K⁺/H⁺ antiporter, Nha1p, is without effect in a sit4 strain, suggesting that Sit4p signals to Nha1p. In summary, the combined activities of Sap155p and Sap185p appear to control the function of Nha1p in K⁺ homeostasis via Sit4p.

Present address: University of Florida College of Medicine, Gainesville, Florida.

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