Cockayne syndrome group B protein enhances elongation by RNA polymerase II
Cockayne syndrome group B protein enhances elongation by RNA polymerase II
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DOI：
10.1073/pnas.94.21.11205
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发表时间：
1997-10-14
影响因子：
11.1
通讯作者：
Sancar, A
中科院分区：
文献类型：
--
作者：
Selby, CP;Sancar, A
科凯恩综合征 (CS) 的特点是身体和精神发育受损。已经确定了两个互补组：CSA 和 CSB。在这里，我们报告 CSB 基因产物增强 RNA 聚合酶 II 的延伸。 CSB 将未损坏模板上的延伸率刺激了约 3 倍。已知位于模板链中的胸腺嘧啶-胸腺嘧啶环丁烷二聚体对转录有很强的阻断作用；将 CSB 添加到封闭的聚合酶中会导致新生转录物中添加一个核苷酸。最后，已知转录因子 IIS 的添加会导致胸腺嘧啶-胸腺嘧啶环丁烷二聚体被阻断的聚合酶消化其新生转录物，并且 CSB 抵消了转录因子 IIS 的这种转录物缩短作用。因此，转录延伸的缺陷可能导致CS表型。
Cockayne syndrome (CS) is characterized by impaired physical and mental development. Two complementation groups, CSA and CSB, have been identified. Here we report that the CSB gene product enhances elongation by RNA polymerase II. CSB stimulated the rate of elongation on an undamaged template by a factor of about 3. A thymine-thymine cyclobutane dimer located in the template strand is known to be a strong block to transcription; Addition of CSB to the blocked polymerase resulted in addition of one nucleotide to the nascent transcript. Finally, addition of transcription factor IIS is known to cause polymerase blocked at a thymine-thymine cyclobutane dimer to digest its nascent transcript, and CSB counteracted this transcript shortening action of transcription factor IIS. Thus a deficiency in transcription elongation may contribute to the CS phenotype.