PDF(Pubmed)
Abstract：
In all cases tested, TFIIIB is responsible for recruiting pol III to its genetic templates. In mammalian cells, RB binds TFIIIB and prevents its interactions with both promoter DNA and pol III, thereby suppressing transcription. As TFIIIB is not recruited to its target genes when bound by RB, the mechanism predicts that pol III-dependent templates will not be occupied by RB; this contrasts with the situation at most genes controlled by RB, where it can be tethered by promoter-bound sequence-specific DNA-binding factors such as E2F. Contrary to this prediction, however, ChIP-seq data reveal the presence of RB in multiple cell types and the related protein p130 at many loci that rely on pol III for their expression, including RMRP, RN7SL, and a variety of tRNA genes. The sets of genes targeted varies according to cell type and growth state. In such cases, recruitment of RB and p130 can be explained by binding of E2F1, E2F4 and/or E2F5. Genes transcribed by pol III had not previously been identified as common targets of E2F family members. The data provide evidence that E2F may allow for the selective regulation of specific non-coding RNAs by RB, in addition to its influence on overall pol III output through its interaction with TFIIIB.
摘要：
在所有测试的情况下，TFIIIB负责向其遗传模板招募polIII。在哺乳动物细胞中,RB结合TFIIIB并阻止其与启动子DNA和polIII的相互作用，从而抑制转录。由于TFIIIB在被RB结合时没有被招募到其靶基因，该机制预测polIII依赖的模板不会被RB占据；这与RB控制的大多数基因的情况相反，其中它可以通过启动子结合的序列特异性DNA结合因子如E2F来连接。与这个预测相反，然而,ChIP-seq数据揭示了RB在多种细胞类型中的存在，以及在许多依赖polIII表达的基因座上的相关蛋白p130，包括RMRP,RN7SL,和多种tRNA基因。靶向基因的集合根据细胞类型和生长状态而变化。在这种情况下,RB和p130的募集可以通过E2F1、E2F4和/或E2F5的结合来解释。polIII转录的基因以前尚未被鉴定为E2F家族成员的常见靶标。数据提供了E2F可以允许RB选择性调节特定的非编码RNA的证据。除了通过其与TFIIIB的相互作用对polIII总输出的影响。
