Vidal M, Buckley A M, Hilger F, Gaber R F
Department of Biochemistry, Molecular Biology and Cell Biology, Northwestern University, Evanston, Illinois 60208.
Genetics. 1990 Jun;125(2):313-20. doi: 10.1093/genetics/125.2.313.
Saccharomyces cerevisiae cells containing a deletion of TRK1, the gene encoding the high affinity potassium transporter, retain only low affinity uptake of this ion and consequently lose the ability to grow in media containing low levels (0.2 mM) of potassium. Using a trk1 delta strain, we selected spontaneous Trk+ pseudorevertants that regained the ability to grow on low concentrations of potassium. The revertants define three unlinked extragenic suppressors of trk1 delta. Dominant RPD2 mutations and recessive rpd1 and rpd3 mutations confer increased potassium uptake in trk1 delta cells. Genetic evidence suggests that RPD2 mutations are alleles of TRK2, the putative low affinity transporter gene, whereas rpd1 and rpd3 mutations increase TRK2 activity: (1) RPD2 mutations are closely linked to trk2, and (2) trk2 mutations are epistatic to both rpd1 and rpd3. rpd1 maps near pho80 on chromosome XV and rpd3 maps on the left arm of chromosome XIV, closely linked to kre1.
酿酒酵母细胞中编码高亲和力钾转运体的基因TRK1缺失后，对该离子仅保留低亲和力摄取，因此失去在含低水平（0.2 mM）钾的培养基中生长的能力。利用trk1Δ菌株，我们筛选出了能在低钾浓度下恢复生长能力的自发Trk +假回复体。这些回复体确定了trk1Δ的三个不连锁的基因外抑制子。显性RPD2突变以及隐性rpd1和rpd3突变使trk1Δ细胞的钾摄取增加。遗传学证据表明，RPD2突变是假定的低亲和力转运体基因TRK2的等位基因，而rpd1和rpd3突变增加了TRK2的活性：（1）RPD2突变与trk2紧密连锁，（2）trk2突变对rpd1和rpd3均呈上位性。rpd1定位于第十五号染色体上靠近pho80的位置，rpd3定位于第十四号染色体的左臂上，与kre1紧密连锁。
