丁型肝炎抗原对RNA聚合酶II延伸的刺激作用。

Stimulation of RNA polymerase II elongation by hepatitis delta antigen.

作者信息

Yamaguchi Y, Filipovska J, Yano K, Furuya A, Inukai N, Narita T, Wada T, Sugimoto S, Konarska M M, Handa H

机构信息

Frontier Collaborative Research Center, Tokyo Institute of Technology, 4259 Nagatsuta, Yokohama 226-8503, Japan.

出版信息

Science. 2001 Jul 6;293(5527):124-7. doi: 10.1126/science.1057925. Epub 2001 May 31.

DOI:10.1126/science.1057925

PMID:11387440

Abstract

Transcription elongation by RNA polymerase II (RNAPII) is negatively regulated by the human factors DRB-sensitivity inducing factor (DSIF) and negative elongation factor (NELF). A 66-kilodalton subunit of NELF (NELF-A) shows limited sequence similarity to hepatitis delta antigen (HDAg), the viral protein required for replication of hepatitis delta virus (HDV). The host RNAPII has been implicated in HDV replication, but the detailed mechanism and the role of HDAg in this process are not understood. We show that HDAg binds RNAPII directly and stimulates transcription by displacing NELF and promoting RNAPII elongation. These results suggest that HDAg may regulate RNAPII elongation during both cellular messenger RNA synthesis and HDV RNA replication.

摘要

RNA聚合酶II（RNAPII）介导的转录延伸受到人类因子DRB敏感性诱导因子（DSIF）和负性延伸因子（NELF）的负调控。NELF的一个66千道尔顿亚基（NELF-A）与丁型肝炎抗原（HDAg）的序列相似性有限，HDAg是丁型肝炎病毒（HDV）复制所需的病毒蛋白。宿主RNAPII参与了HDV复制，但该过程的详细机制以及HDAg在此过程中的作用尚不清楚。我们发现，HDAg直接结合RNAPII，并通过取代NELF和促进RNAPII延伸来刺激转录。这些结果表明，HDAg可能在细胞信使RNA合成和HDV RNA复制过程中调节RNAPII延伸。