Egyházi E, Ossoinak A, Pigon A, Holmgren C, Lee J M, Greenleaf A L
Karolinska Institutet, Department of Cell and Molecular Biology, Laboratory of Medical Cell Biology, S-171 77 Stockholm, Sweden.
Chromosoma. 1996 Mar;104(6):422-33. doi: 10.1007/BF00352266.
Using polytene chromosomes of salivary gland cells of Chironomus tentans, phosphorylation state-sensitive antibodies and the transcription and protein kinase inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), we have visualized the chromosomal distribution of RNA polymerase II (pol II) with hypophosphorylated (pol IIA) and hyperphosphorylated (pol II0) carboxyl-terminal repeat domain (CTD). DRB blocks labeling of the CTD with 32Pi within minutes of its addition, and nuclear pol II0 is gradually converted to IIA; this conversion parallels the reduction in transcription of protein-coding genes. DRB also alters the chromosomal distribution of II0: there is a time-dependent clearance from chromosomes of phosphoCTD (PCTD) after addition of DRB, which coincides in time with the completion and release of preinitiated transcripts. Furthermore, the staining of smaller transcription units is abolished before that of larger ones. The staining pattern of chromosomes with anti-CTD antibodies is not detectably influenced by the DRB treatment, indicating that hypophosphorylated pol IIA is unaffected by the transcription inhibitor. Microinjection of synthetic heptapeptide repeats, anti-CTD and anti-PCTD antibodies into salivary gland nuclei hampered the transcription of BR2 genes, indicating the requirement for CTD and PCTD in transcription in living cells. The results demonstrate that in vivo the protein kinase effector DRB shows parallel effects on an early step in gene transcription and the process of pol II hyperphosphorylation. Our observations are consistent with the proposal that the initiation of productive RNA synthesis is CTD-phosphorylation dependent and also with the idea that the gradual dephosphorylation of transcribing pol II0 is coupled to the completion of nascent pol II gene transcripts.
利用摇蚊的唾液腺细胞多线染色体、磷酸化状态敏感抗体以及转录和蛋白激酶抑制剂5,6 - 二氯 - 1 - β - D - 呋喃核糖基苯并咪唑(DRB),我们观察到了具有低磷酸化(pol IIA)和高磷酸化(pol II0)羧基末端重复结构域(CTD)的RNA聚合酶II(pol II)在染色体上的分布情况。加入DRB后几分钟内,它就能阻断32Pi对CTD的标记,并且细胞核中的pol II0会逐渐转化为IIA;这种转化与蛋白质编码基因转录的减少同步。DRB还会改变II0在染色体上的分布:加入DRB后,磷酸化CTD(PCTD)会随着时间从染色体上清除,这与起始转录本的完成和释放时间一致。此外,较小转录单位的染色在较大转录单位之前就消失了。用抗CTD抗体对染色体进行染色,其染色模式并未受到DRB处理的明显影响,这表明低磷酸化的pol IIA不受转录抑制剂的影响。将合成的七肽重复序列、抗CTD和抗PCTD抗体显微注射到唾液腺细胞核中会阻碍BR2基因的转录,这表明在活细胞转录过程中CTD和PCTD是必需的。结果表明,在体内蛋白激酶效应物DRB对基因转录的早期步骤和pol II高磷酸化过程具有平行作用。我们的观察结果与以下观点一致,即有成效的RNA合成起始依赖于CTD磷酸化,也与正在转录的pol II0的逐渐去磷酸化与新生pol II基因转录本的完成相关这一观点一致。