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Eukaryot Cell. 2005 Jun;4(6):1041-9.

Ability of Sit4p to promote K+ efflux via Nha1p is modulated by Sap155p and Sap185p.

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1
Department of Biology, Georgetown University, 406 Reiss Science Center, Box 571229, Washington, DC 20057-1229, USA. rosenwaa@georgetown.edu

Abstract

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 sit4Delta strains. However, overexpression of the Na+-K+/H+ antiporter, Nha1p, is without effect in a sit4Delta 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.

PMID:
15947196
PMCID:
PMC1151994
DOI:
10.1128/EC.4.6.1041-1049.2005
[Indexed for MEDLINE]
Free PMC Article
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