title: Ability of Sit4p to promote K+ efflux via Nha1p is modulated by Sap155p and Sap185p.
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.
authors.affiliation: Department of Biology, Georgetown University, 406 Reiss Science Center, Box 571229, Washington, DC 20057-1229, USA. rosenwaa@georgetown.edu
authors.forename: Cara Marie A
authors.initials: CM
authors.lastname: Manlandro
authors.forename: Devon H
authors.initials: DH
authors.lastname: Haydon
authors.forename: Anne G
authors.initials: AG
authors.lastname: Rosenwald
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000071183:Autophagy-Related Proteins; D002352:Carrier Proteins / Q000378:metabolism*; D027682:Cation Transport Proteins / Q000378:metabolism*; D005656:Fungal Proteins / Q000378:metabolism*; D017353:Gene Deletion; D006921:Hygromycin B / Q000494:pharmacology; D007700:Kinetics; D008565:Membrane Proteins / Q000378:metabolism*; D010749:Phosphoprotein Phosphatases / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D054648:Protein Phosphatase 2; D017413:Ribonucleoprotein, U2 Small Nuclear / Q000378:metabolism*; D012413:Rubidium / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D029701:Saccharomyces cerevisiae Proteins / Q000378:metabolism*; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism*; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: C498649:ATG16 protein, S cerevisiae; D048868:Adaptor Proteins, Signal Transducing; D000071183:Autophagy-Related Proteins; D002352:Carrier Proteins; D027682:Cation Transport Proteins; D005656:Fungal Proteins; D008565:Membrane Proteins; C000631624:NHA1 protein, S cerevisiae; D010750:Phosphoproteins; D017413:Ribonucleoprotein, U2 Small Nuclear; C491800:SAP155 protein, S cerevisiae; D029701:Saccharomyces cerevisiae Proteins; D017923:Sodium-Hydrogen Exchangers; D014157:Transcription Factors; D006921:Hygromycin B; D010749:Phosphoprotein Phosphatases; D054648:Protein Phosphatase 2; C104343:SIT4 protein, S cerevisiae; D012413:Rubidium; D011188:Potassium