Bertl A, Anderson J A, Slayman C L, Sentenac H, Gaber R F
Department of Cellular and Molecular Physiology, Yale University, New Haven, CT 06510, USA.
Folia Microbiol (Praha). 1994;39(6):507-9. doi: 10.1007/BF02814074.
Disruption of genes encoding endogenous transport proteins in Saccharomyces cerevisiae has facilitated the recent cloning, by functional expression, of cDNAs encoding K+ channels and amino acid transporters from the plant Arabidopsis thaliana [1-4]. In the present study, we demonstrate in whole-cell patch clamp experiments that the inability of trk1deltatrk2delta mutants of S. cerevisiae to grow on submillimolar K+ correlates with the lack of K+ inward currents, which are present in wild-type cells, and that transformation of the trk1deltatrk2delta double-deletion mutant with KAT1 from Arabidopsis thaliana restores this phenotype by encoding a plasma membrane protein that allows large K+ inward currents. Similar K+ inward currents are induced by transformation of a trk1 mutant with AKT1 from A. thaliana.
破坏酿酒酵母中编码内源性转运蛋白的基因,有助于最近通过功能表达克隆来自植物拟南芥的编码钾离子通道和氨基酸转运体的cDNA[1-4]。在本研究中,我们在全细胞膜片钳实验中证明,酿酒酵母的trk1Δtrk2Δ突变体在亚毫摩尔钾离子浓度下无法生长,这与野生型细胞中存在的钾离子内向电流缺失有关,并且用拟南芥的KAT1转化trk1Δtrk2Δ双缺失突变体,通过编码一种允许大量钾离子内向电流的质膜蛋白恢复了这种表型。用拟南芥的AKT1转化trk1突变体也诱导了类似的钾离子内向电流。