Rose K M, Bell L E, Jacob S T
Department of Pharmacology, Milton S. Hershey Medical Centre, Pennsylvania State University, College of Medicine, Hershey, Pennsylvania 17033, USA.
Nature. 1977 May 12;267(5607):178-80. doi: 10.1038/267178a0.
It has been established that many eukaryotic mRNAs contain poly(adenylic acid) tracts at their 3'-termini. The polyadenylation of mRNA occurs post-transcriptionally in the nucleus as a rapid, initial addition of 100-200 adenylate residues to the pre-mRNA (ref. 1). Subsequently, a slower chain extension (6-8 bases) of the poly(A) tail seems to occur both in the nucleus and in the cytoplasm. The initial polyadenylation reaction can be specifically inhibited by the drug cordycepin (3'-deoxyadenosine) in cell culture, presumably by its conversion to the triphosphate analogue which acts as a competitive inhibitor of poly(A) polymerase. Cordycepin, however, has little effect on the slower poly(A) extension reaction or on the formation of mRNA precursor molecules; but it can inhibit rRNA synthesis. Contrary to the in vitro observations, cordycepin 5'-triphosphate (3'dATP) is not a specific inhibitor of poly(A) synthesis in vivo, relative to RNA synthesis, and RNA polymerase I (which synthesises rRNA) is actually less sensitive to inhibition by 3'dATP than RNA polymerase II (ref. 10) (which is presumed to be involved in the synthesis of mRNA). Since nuclear poly(A) polymerase occurs in two functional states as 'free' and 'chromatin-bound' forms, we reasoned that if the chromatin-associated poly(A) polymerase were involved in the initial polyadenylation of mRNA, it might be selectively inhibited by 3'dATP. The present studies, designed to test such an idea, demonstrate that, as in vivo, the initial polyadenylation reaction can be selectively inhibited in vitro by low levels of 3'dATP. These data also show that higher levels of 3'dATP can inhibit RNA synthesis, 'chromatin-bound' RNA polymerase I activity being significantly more sensitive than the 'bound' RNA polymerase II activity.
现已确定,许多真核生物mRNA在其3'末端含有聚腺苷酸序列。mRNA的聚腺苷酸化在细胞核内转录后发生,是一个快速的过程,首先在mRNA前体上添加100 - 200个腺苷酸残基(参考文献1)。随后,聚(A)尾的链延伸较慢(6 - 8个碱基),似乎在细胞核和细胞质中都会发生。在细胞培养中,药物虫草素(3'-脱氧腺苷)可特异性抑制初始聚腺苷酸化反应,推测是通过将其转化为三磷酸类似物,该类似物作为聚(A)聚合酶的竞争性抑制剂发挥作用。然而,虫草素对较慢的聚(A)延伸反应或mRNA前体分子的形成影响很小;但它可以抑制rRNA合成。与体外观察结果相反,相对于RNA合成,虫草素5'-三磷酸(3'dATP)在体内并非聚(A)合成的特异性抑制剂,而且RNA聚合酶I(合成rRNA)实际上比RNA聚合酶II(推测参与mRNA合成)对3'dATP抑制的敏感性更低(参考文献10)。由于细胞核聚(A)聚合酶以“游离”和“与染色质结合”两种功能状态存在,我们推测,如果与染色质相关的聚(A)聚合酶参与mRNA的初始聚腺苷酸化,它可能会被3'dATP选择性抑制。旨在验证这一想法的当前研究表明,与体内情况一样,低水平的3'dATP在体外可选择性抑制初始聚腺苷酸化反应。这些数据还表明,较高水平的3'dATP可抑制RNA合成,“与染色质结合的”RNA聚合酶I活性比“结合的”RNA聚合酶II活性对其更敏感。