White R J, Gottlieb T M, Downes C S, Jackson S P
Wellcome/CRC Institute, University of Cambridge, United Kingdom.
Mol Cell Biol. 1995 Dec;15(12):6653-62. doi: 10.1128/MCB.15.12.6653.
Inactivation of the TATA-binding protein-containing complex TFIIIB contributes to the mitotic repression of RNA polymerase III transcription, both in frogs and in humans (J. M. Gottesfeld, V. J. Wolf, T. Dang, D. J. Forbes, and P. Hartl, Science 263:81-84, 1994; R. J. White, T. M. Gottlieb, C. S. Downes, and S. P. Jackson, Mol. Cell. Biol. 15:1983-1992, 1995). Using extracts of synchronized proliferating HeLa cells, we show that TFIIIB activity remains low during the early part of G1 phase and increases only gradually as cells approach S phase. As a result, the transcription of all class III genes tested is significantly less active in early G1 than it is in S or G2 phase, both in vitro and in vivo. The increased activity of TFIIIB as cells progress through interphase appears to be due to changes in the TATA-binding protein-associated components of this complex. The data suggest that TFIIIB is an important target for the cell cycle regulation of RNA polymerase III transcription during both mitosis and interphase of actively proliferating HeLa cells.
在青蛙和人类中，含TATA结合蛋白的复合物TFIIIB的失活都有助于有丝分裂时RNA聚合酶III转录的抑制（J.M.戈特斯费尔德、V.J.沃尔夫、T.当、D.J.福布斯和P.哈特尔，《科学》263:81 - 84，1994；R.J.怀特、T.M.戈特利布、C.S.唐斯和S.P.杰克逊，《分子细胞生物学》15:1983 - 1992，1995）。利用同步化增殖的HeLa细胞提取物，我们发现TFIIIB活性在G1期早期保持较低水平，仅在细胞接近S期时才逐渐增加。因此，无论是在体外还是体内，所有测试的III类基因的转录在G1期早期的活性都明显低于S期或G2期。随着细胞在间期的进展，TFIIIB活性的增加似乎是由于该复合物中与TATA结合蛋白相关的成分发生了变化。数据表明，在活跃增殖的HeLa细胞的有丝分裂和间期，TFIIIB都是RNA聚合酶III转录细胞周期调控的重要靶点。
