A model of repression: CTD analogs and PIE-1 inhibit transcriptional elongation by P-TEFb

被引：90

作者：

Zhang, F

Barboric, M ^{[1
]}

Blackwell, TK

Peterlin, BM

机构：

[1] Univ Calif San Francisco, Rosalind Russell Med Res Ctr, Dept Med, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Rosalind Russell Med Res Ctr, Dept Microbiol, San Francisco, CA 94143 USA

[3] Univ Calif San Francisco, Rosalind Russell Med Res Ctr, Dept Immunol, San Francisco, CA 94143 USA

[4] Univ Ljubljana, Fac Med, Inst Biochem, Ljubljana 61000, Slovenia

[5] Harvard Univ, Sch Med, Ctr Blood Res, Boston, MA 02115 USA

[6] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

来源：

GENES & DEVELOPMENT | 2003年 / 17卷 / 06期

关键词：

P-TEFb; CTD; PIE-1; transcription; repression; elongation;

D O I：

10.1101/gad.1068203

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The positive transcription elongation factor b (P-TEFb) contains cyclin T1 (CycT1) and cyclin-dependent kinase 9 (Cdk9). For activating the expression of eukaryotic genes, the histidine-rich sequence in CycT1 binds the heptapeptide repeats in the C-terminal domain (CTD) of RNA polymerase II (RNAPII), whereupon Cdk9 phosphorylates the CTD. We found that alanine-substituted heptapeptide repeats that cannot be phosphorylated also bind CycT1. When placed near transcription units, these CTD analogs block effects of P-TEFb. Remarkably, the transcriptional repressor PIE-1 from Caenorhabditis elegans behaves analogously. It binds CycT1 via an alanine-containing heptapeptide repeat and inhibits transcriptional elongation. Thus, our findings reveal a new mechanism by which repressors inhibit eukaryotic transcription.

引用

页码：748 / 758

页数：11

共 53 条

[1] NF-κB binds P-TEFb to stimulate transcriptional elongation by RNA polymerase II [J].