p53 represses the transcription of snRNA genes by preventing the formation of little elongation complex
p53 represses the transcription of snRNA genes by preventing the formation of little elongation complex
复制标题
DOI：
10.1016/j.bbagrm.2016.06.001
复制
发表时间：
2016-08-01
影响因子：
4.7
通讯作者：
Hatakeyama, Shigetsugu
中科院分区：
文献类型：
--
作者：
Anwar, Delnur;Takahashi, Hidehisa;Hatakeyama, Shigetsugu
RNA聚合酶II（Pol II）对转录的调节对于多种细胞功能是重要的。ELL/EAF的小延伸复合物（LEC）被发现是所需的Pol II依赖的小核RNA（snRNA）基因的转录。结果表明，抑癌基因p53与ELL相互作用，抑制ELL的转录延长活性。在这里，我们发现，p53抑制LEC中ELL/EAF和ICE 1之间的相互作用，从而p53通过抑制LEC功能抑制Pol II依赖的snRNA基因的转录。此外，通过紫外线（UV）照射诱导p53表达降低了ICE 1在Pol II依赖性snRNA基因上的占有率。与结果一致，敲除p53增加了snRNA基因的表达和Pol II和LEC组分在snRNA基因处的占据。我们的研究结果表明，p53干扰ELL/EAF和ICE 1之间的相互作用，并通过Pol II抑制snRNA基因的转录。(C)© 2016 Elsevier B. V.版权所有。
The regulation of transcription by RNA polymerase II (Pol II) is important for a variety of cellular functions. ELL/EAF-containing little elongation complex (LEC) was found to be required for transcription of Pol II-dependent small nuclear RNA (snRNA) genes. It was shown that the tumor suppressor p53 interacts with ELL and inhibits transcription elongation activity of ELL Here, we show that p53 inhibits interaction between ELL/EAF and ICE1 in LEC and thereby p53 represses transcription of Pol II-dependent snRNA genes through inhibiting LEC function. Furthermore, induction of p53 expression by ultraviolet (UV) irradiation decreases the occupancy of ICE1 at Pol II-dependent snRNA genes. Consistent with the results, knockdown of p53 increased both the expression of snRNA genes and the occupancy of Pol II and components of LEC at snRNA genes. Our results indicate that p53 interferes with the interaction between ELL/EAF and ICE1 and represses transcription of snRNA genes by Pol II. (C) 2016 Elsevier B.V. All rights reserved.