Chouinard S W, Wilson G F, Schlimgen A K, Ganetzky B
Laboratory of Genetics, University of Wisconsin, Madison 53706, USA.
Proc Natl Acad Sci U S A. 1995 Jul 18;92(15):6763-7. doi: 10.1073/pnas.92.15.6763.
Genetic and physiological studies of the Drosophila Hyperkinetic (Hk) mutant revealed defects in the function or regulation of K+ channels encoded by the Shaker (Sh) locus. The Hk polypeptide, determined from analysis of cDNA clones, is a homologue of mammalian K+ channel beta subunits (Kv beta). Coexpression of Hk with Sh in Xenopus oocytes increases current amplitudes and changes the voltage dependence and kinetics of activation and inactivation, consistent with predicted functions of Hk in vivo. Sequence alignments show that Hk, together with mammalian Kv beta, represents an additional branch of the aldo-keto reductase superfamily. These results are relevant to understanding the function and evolutionary origin of Kv beta.
对果蝇“运动过强”（Hk）突变体的遗传学和生理学研究揭示了由“振子”（Sh）基因座编码的钾离子通道在功能或调节方面的缺陷。通过对cDNA克隆的分析确定，Hk多肽是哺乳动物钾离子通道β亚基（Kvβ）的同源物。在非洲爪蟾卵母细胞中，Hk与Sh共同表达会增加电流幅度，并改变激活和失活的电压依赖性及动力学，这与Hk在体内的预测功能一致。序列比对表明，Hk与哺乳动物Kvβ一起，代表了醛酮还原酶超家族的一个额外分支。这些结果对于理解Kvβ的功能和进化起源具有重要意义。
