Van Haastert P J
Department of Biochemistry, University of Groningen, The Netherlands.
Biochem J. 1994 Oct 15;303 ( Pt 2)(Pt 2):539-45. doi: 10.1042/bj3030539.
Dictyostelium discoideum cells contain cell surface cyclic AMP (cAMP) receptors that bind cAMP as a first messenger and intracellular cAMP receptors that bind cAMP as a second messenger. Prolonged incubation of Dictyostelium cells with cAMP induces a sequential process of phosphorylation, sequestration and down-regulation of the surface receptors. The role of intracellular cAMP in down-regulation of surface receptors was investigated. Down-regulation of receptors does not occur under conditions that specifically inhibit the formation of intracellular cAMP (the drug caffeine or mutant cells lacking adenylate cyclase) or conditions that inhibit the function of intracellular cAMP (mutants lacking protein kinase A activity). Cell-permeable non-hydrolysable cAMP derivatives were used to investigate further the requirement of intracellular cAMP for down-regulation. The Sp isomer of 6-thioethylpurineriboside 3',5'-phosphorothioate (6SEth-cPuMPS) does not bind to the surface receptor, enters the cell and has relative high affinity for protein kinase A. 6SEth-cPuMPS alone has no effect on down-regulation. However, together with an agonist of the surface receptor, the analogue induces down-regulation in caffeine-treated wild-type cells and in mutant cells lacking adenylate cyclase, but not in mutant cells lacking protein kinase A. These results indicate that intracellular cAMP formation and activation of protein kinase A are essential for down-regulation of the surface cAMP receptor.
盘基网柄菌细胞含有细胞表面环磷酸腺苷(cAMP)受体,其作为第一信使结合cAMP,以及细胞内cAMP受体,其作为第二信使结合cAMP。用cAMP长时间孵育盘基网柄菌细胞会诱导表面受体的磷酸化、隔离和下调的连续过程。研究了细胞内cAMP在表面受体下调中的作用。在特异性抑制细胞内cAMP形成的条件下(药物咖啡因或缺乏腺苷酸环化酶的突变细胞)或抑制细胞内cAMP功能的条件下(缺乏蛋白激酶A活性的突变体),受体不会发生下调。使用可渗透细胞的不可水解cAMP衍生物进一步研究细胞内cAMP对下调的需求。6-硫代乙基嘌呤核糖苷3',5'-硫代磷酸酯(6SEth-cPuMPS)的Sp异构体不与表面受体结合,进入细胞并对蛋白激酶A具有相对高的亲和力。单独的6SEth-cPuMPS对下调没有影响。然而,与表面受体的激动剂一起,该类似物在咖啡因处理的野生型细胞和缺乏腺苷酸环化酶的突变细胞中诱导下调,但在缺乏蛋白激酶A的突变细胞中则不会。这些结果表明,细胞内cAMP的形成和蛋白激酶A的激活对于表面cAMP受体的下调至关重要。