Manlandro Cara Marie A, Haydon Devon H, Rosenwald Anne G
Department of Biology, Georgetown University, 406 Reiss Science Center, Box 571229, Washington, DC 20057-1229, USA.
Eukaryot Cell. 2005 Jun;4(6):1041-9. doi: 10.1128/EC.4.6.1041-1049.2005.
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 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.
我们在此证明，在酿酒酵母中，SAP155编码一种K⁺外流的负调节因子。SAP155的过表达会减少外流，而缺失则会增加外流。相反，一种名为SAP185的SAP155同源物编码K⁺外流的正调节因子：SAP185的过表达会增加外流，而缺失则会减少外流。另外两个同源物SAP4和SAP190对K⁺稳态没有影响。SAP155和SAP185发挥功能都需要SIT4的存在，SIT4编码一种对细胞周期中G1-S转变很重要的PP2A样磷酸酶。外向整流K⁺通道Tok1p或假定的质膜K⁺/H⁺反向转运蛋白Kha1p的过表达，都会增加野生型和sit4Δ菌株中的外流。然而，Na⁺-K⁺/H⁺反向转运蛋白Nha1p的过表达在sit4Δ菌株中没有作用，这表明Sit4p向Nha1p发出信号。总之，Sap155p和Sap185p的联合活性似乎通过Sit4p控制Nha1p在K⁺稳态中的功能。
