Liao Yanling, Moir Robyn D, Willis Ian M
Department of Biochemistry, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, USA.
Mol Cell Biol. 2006 Aug;26(16):5946-56. doi: 10.1128/MCB.00689-06.
The binding of Brf1 to the tetratricopeptide repeat (TPR)-containing transcription factor IIIC (TFIIIC) subunit (Tfc4) represents a rate-limiting step in the ordered assembly of the RNA polymerase III initiation factor TFIIIB. Tfc4 contains multiple binding sites for Brf1 within its amino terminus and adjacent TPR arrays, but the access of Brf1 to these sites is limited by autoinhibition. Moreover, the Brf1 binding sites in Tfc4 overlap with sites important for the subsequent recruitment of another TFIIIB subunit, Bdp1, implying that repositioning of Brf1 is required after its initial interaction with Tfc4. As a starting point for dissecting the steps in TFIIIC-directed assembly of TFIIIB, we conducted yeast two-hybrid screens of Brf1 peptide libraries against different TPR-containing Tfc4 fragments. Short, biochemically active peptides were identified in three distinct regions of Brf1. Two peptides defined conserved but distal regions of Brf1 that participate in stable binding of Brf1 to TFIIIC-DNA. Remarkably, a third peptide that binds specifically to TPR6-9 of Tfc4 was found to promote the formation of both TFIIIC-DNA and Brf1-TFIIIC-DNA complexes and to reduce the mobility of these complexes in native gels. The data are consistent with this peptide causing a conformational change in TFIIIC that overcomes Tfc4 autoinhibition of Brf1 binding and suggest a structural model for the Brf1-Tfc4 interaction.
Brf1与含四肽重复序列(TPR)的转录因子IIIC(TFIIIC)亚基(Tfc4)的结合是RNA聚合酶III起始因子TFIIIB有序组装过程中的限速步骤。Tfc4在其氨基末端和相邻的TPR阵列中含有多个Brf1结合位点,但Brf1对这些位点的访问受到自身抑制的限制。此外,Tfc4中的Brf1结合位点与另一个TFIIIB亚基Bdp1后续招募的重要位点重叠,这意味着Brf1在与Tfc4初始相互作用后需要重新定位。作为剖析TFIIIC指导的TFIIIB组装步骤的起点,我们针对不同的含TPR的Tfc4片段对Brf1肽库进行了酵母双杂交筛选。在Brf1的三个不同区域鉴定出了短的、具有生化活性的肽。两个肽定义了Brf1的保守但远端区域,这些区域参与Brf1与TFIIIC-DNA的稳定结合。值得注意的是,发现一个与Tfc4的TPR6-9特异性结合的第三个肽能促进TFIIIC-DNA和Brf1-TFIIIC-DNA复合物的形成,并降低这些复合物在天然凝胶中的迁移率。这些数据与该肽导致TFIIIC构象变化从而克服Tfc4对Brf1结合的自身抑制作用一致,并提出了Brf1-Tfc4相互作用的结构模型。