Reardon J T, Ge H, Gibbs E, Sancar A, Hurwitz J, Pan Z Q
Department of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill 27599, USA.
Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6482-7. doi: 10.1073/pnas.93.13.6482.
Transcription factor IIH (TFIIH) is a multisubunit protein complex essential for both the initiation of RNA polymerase class II (pol II)-catalyzed transcription and nucleotide excision repair of DNA. Recent studies have shown that TFIIH copurifies with the cyclin-dependent kinase (cdk)-activating kinase complex (CAK) that includes cdk7, cyclin H, and p36/MAT1. Here we report the isolation of two TFIIH-related complexes: TFIIH* and ERCC2/CAK. TFIIH* consists of a subset of the TFIIH complex proteins including ERCC3 (XPB), p62, p44, p41, and p34 but is devoid of detectable levels of ERCC2 (XPD) and CAK. ERCC2/CAK was isolated as a complex that exhibits CAK activity that cosediments with the three CAK components (cdk7, cyclin H, and p36/MAT1) as well as the ERCC2 (XPD) protein. TFIIH* can support pol II-catalyzed transcription in vitro with lower efficiency compared with TFIIH. This TFIIH*-dependent transcription reaction was stimulated by ERCC2/CAK. The ERCC2/CAK and TFIIH* complexes are each active in DNA repair as shown by their ability to complement extracts prepared from ERCC2 (XPD)- and ERCC3 (XPB)-deficient cells, respectively, in supporting the excision of DNA containing a cholesterol lesion. These data suggest that TFIIH* and ERCC2/CAK interact to form the TFIIH holoenzyme capable of efficiently assembling the pol II transcription initiation complex and directly participating in excision repair reactions.
转录因子IIH(TFIIH)是一种多亚基蛋白复合体,对于RNA聚合酶II(pol II)催化的转录起始和DNA核苷酸切除修复均至关重要。最近的研究表明,TFIIH与包含细胞周期蛋白依赖性激酶(cdk)激活激酶复合体(CAK)共纯化,CAK包括cdk7、细胞周期蛋白H和p36/MAT1。在此,我们报告了两种与TFIIH相关的复合体的分离:TFIIH和ERCC2/CAK。TFIIH由TFIIH复合体蛋白的一个子集组成,包括ERCC3(XPB)、p62、p44、p41和p34,但未检测到可检测水平的ERCC2(XPD)和CAK。ERCC2/CAK作为一种具有CAK活性的复合体被分离出来,它与三种CAK成分(cdk7、细胞周期蛋白H和p36/MAT1)以及ERCC2(XPD)蛋白一起沉降。与TFIIH相比,TFIIH在体外支持pol II催化的转录效率较低。这种依赖TFIIH的转录反应受到ERCC2/CAK的刺激。ERCC2/CAK和TFIIH复合体在DNA修复中均具有活性,分别通过它们补充从ERCC2(XPD)和ERCC3(XPB)缺陷细胞制备的提取物以支持切除含胆固醇损伤的DNA的能力得以证明。这些数据表明,TFIIH和ERCC2/CAK相互作用形成能够有效组装pol II转录起始复合体并直接参与切除修复反应的TFIIH全酶。