Rahmsdorf H J, Pai S H, Ponta H, Herrlich P, Roskoski R, Schweiger M, Studier F W
Proc Natl Acad Sci U S A. 1974 Feb;71(2):586-9. doi: 10.1073/pnas.71.2.586.
After bacteriophage T7 infection, a protein kinase (EC 2.7.1.37; ATP:protein phosphotransferase) activity can be demonstrated in E. coli in vivo by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography. Cell-free extracts catalyzed the transfer of the terminal phosphoryl group of [(gamma)-(32)P]ATP to endogenous protein acceptor or to added histone. The bond between phosphate and protein shows the characteristics of serine phosphate: it is stable in 1 N HCl (100 degrees ) and cleaved by 1 N KOH (37 degrees ) and by alkaline phosphatase treatment. Moreover, after partial acid hydrolysis, radiophosphate migrates with marker O-phosphoserine on polyethyleneimine-cellulose thin-layer chromatograms. Enzyme activity in uninfected cells is negligible. Ultraviolet irradiation of the phage genome prevents the appearance of the protein kinase; irradiation of the host genome does not. The enzyme activity occurs 4 min after infection and its gene maps in the early region (promoter proximal to gene 1). Ribosomal proteins are phosphorylated in vivo and are substrates in vitro. Enzyme activity in vitro is not changed by addition of cyclic AMP or cyclic GMP.
在噬菌体T7感染后,通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和放射自显影技术,可在体内大肠杆菌中检测到一种蛋白激酶(EC 2.7.1.37;ATP:蛋白磷酸转移酶)活性。无细胞提取物催化[(γ)-(32)P]ATP的末端磷酰基转移至内源性蛋白受体或添加的组蛋白上。磷酸与蛋白之间的键呈现出丝氨酸磷酸的特征:在1 N HCl(100℃)中稳定,在1 N KOH(37℃)及碱性磷酸酶处理下可裂解。此外,部分酸水解后,放射性磷酸盐在聚乙烯亚胺-纤维素薄层层析图谱上与标记的O-磷酸丝氨酸一同迁移。未感染细胞中的酶活性可忽略不计。噬菌体基因组的紫外线照射可阻止蛋白激酶的出现;宿主基因组的照射则不会。酶活性在感染后4分钟出现,其基因定位于早期区域(基因1近端的启动子)。核糖体蛋白在体内被磷酸化,且在体外是底物。体外添加环磷酸腺苷或环磷酸鸟苷不会改变酶活性。