Li W, Luan S, Schreiber S L, Assmann S M
Biological Laboratory, Harvard University, Cambridge, Massachusetts 02138.
Plant Physiol. 1994 Nov;106(3):957-61. doi: 10.1104/pp.106.3.957.
Whole-cell patch-clamp recordings from Vicia faba mesophyll protoplasts reveal that outward K+ current is increased in a dose-dependent fashion by intracellular application of cAMP. The enhancement of the outward current by cAMP is specific and it cannot be mimicked by a series of nucleotides that includes AMP, cGMP, and GMP. The enhancement is evoked by micromolar concentrations of cAMP in the presence of the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine. PKI or Walsh inhibitor, a specific peptide inhibitor of cAMP-dependent protein kinase (PKA), inhibits the outward K+ current. Adenosine 3',5'-phosphothioate, a competitive inhibitor of PKA, has a similar effect. Conversely, the catalytic subunit of PKA (cAMP independent) from bovine brain enhances the magnitude of the outward K+ current in the absence of added cAMP. Our results indicate that cAMP modulates K+ channel activity in mesophyll cells and suggest that this modulation occurs through a cAMP-regulated protein kinase.
蚕豆叶肉原生质体的全细胞膜片钳记录显示，通过细胞内施加环磷酸腺苷（cAMP），外向钾离子电流以剂量依赖方式增加。cAMP对外向电流的增强作用具有特异性，一系列核苷酸（包括腺苷一磷酸（AMP）、环磷酸鸟苷（cGMP）和鸟苷一磷酸（GMP））无法模拟这种增强作用。在磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤存在的情况下，微摩尔浓度的cAMP可引发这种增强作用。PKI或沃尔什抑制剂（一种环磷酸腺苷依赖性蛋白激酶（PKA）的特异性肽抑制剂）可抑制外向钾离子电流。PKA的竞争性抑制剂3',5'-硫代磷酸腺苷具有类似作用。相反，来自牛脑的PKA催化亚基（不依赖cAMP）在未添加cAMP的情况下可增强外向钾离子电流的幅度。我们的结果表明，cAMP调节叶肉细胞中的钾离子通道活性，并提示这种调节通过cAMP调节的蛋白激酶发生。
