Li Shisheng, Ding Baojin, Chen Runqiang, Ruggiero Christine, Chen Xuefeng
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.
Mol Cell Biol. 2006 Dec;26(24):9430-41. doi: 10.1128/MCB.01656-06. Epub 2006 Oct 9.
Rpb9, a small nonessential subunit of RNA polymerase II, has been shown to have multiple transcription-related functions in Saccharomyces cerevisiae. These functions include promoting transcription elongation and mediating a subpathway of transcription-coupled repair (TCR) that is independent of Rad26, the homologue of human Cockayne syndrome complementation group B protein. Rpb9 is composed of three distinct domains: the N-terminal Zn1, the C-terminal Zn2, and the central linker. Here we show that the Zn1 and linker domains are essential, whereas the Zn2 domain is almost dispensable, for both transcription elongation and TCR functions. Impairment of transcription elongation, which does not dramatically compromise Rad26-mediated TCR, completely abolishes Rpb9-mediated TCR. Furthermore, Rpb9 appears to be dispensable for TCR if its transcription elongation function is compensated for by removing a transcription repression/elongation factor. Our data suggest that the transcription elongation function of Rpb9 is involved in TCR.
Rpb9是RNA聚合酶II的一个非必需小亚基,已证实在酿酒酵母中具有多种与转录相关的功能。这些功能包括促进转录延伸以及介导转录偶联修复(TCR)的一个独立于Rad26(人类科凯恩综合征互补组B蛋白的同源物)的子途径。Rpb9由三个不同结构域组成:N端的Zn1、C端的Zn2和中间的连接区。我们在此表明,对于转录延伸和TCR功能而言,Zn1和连接区结构域是必需的,而Zn2结构域几乎是可有可无的。转录延伸受损虽不会显著损害Rad26介导的TCR,但会完全消除Rpb9介导的TCR。此外,如果通过去除一个转录抑制/延伸因子来补偿其转录延伸功能,那么Rpb9对于TCR似乎是可有可无的。我们的数据表明,Rpb9的转录延伸功能参与了TCR。