The export factor Yra1 modulates mRNA 3' end processing.

The export factor Yra1 modulates mRNA 3' end processing.
复制标题

DOI:
10.1038/nsmb.2126
复制
发表时间:
2011-09-25
影响因子:
16.8
通讯作者:
--
中科院分区:
生物学1区
文献类型:
--
作者:

文献摘要

参考文献

被引文献

相似文献

酵母mRNA输出接头Yra1结合裂解-聚腺苷化因子CF1A的Pcf11亚基,将输出连接到3 '端形成。我们发现这种相互作用的一个令人惊讶的结果是Yra1影响卵裂-聚腺苷酸化。Yra1与CF1A亚基Clp1竞争,与Pcf11结合,过量的Yra1在体外抑制3 '加工。基因3 '端Yra1的释放与Clp1的募集一致,Yra1的缺失增强了某些基因内Clp1的募集。这些结果表明,CF1A不一定作为一个完整的单位被招募,相反,Clp1可以在Yra1调节的过程中被共转录纳入。Yra1耗损导致poly(A)位点选择的广泛变化,特别是在效率元件发散位置的位点。我们提出Yra1调节裂解-聚腺苷化的一种方式是通过影响CF1A/ b3 '加工因子的共转录组装。
The yeast mRNA export adaptor Yra1 binds the Pcf11 subunit of cleavage-polyadenylation factor CF1A linking export to 3’-end formation. We found a surprising consequence of this interaction is that Yra1 influences cleavage-polyadenylation. Yra1 competes with the CF1A subunit, Clp1, for binding to Pcf11, and excess Yra1 inhibits 3’ processing in vitro. Release of Yra1 at the 3’ ends of genes coincides with recruitment of Clp1, and depletion of Yra1 enhances Clp1 recruitment within some genes. These results suggest that CF1A is not necessarily recruited as a complete unit, but instead Clp1 can be incorporated co-transcriptionally in a process regulated by Yra1. Yra1 depletion causes widespread changes in poly(A) site choice particularly at sites where the efficiency element is divergently positioned. We propose that one way Yra1 modulates cleavage-polyadenylation is by influencing co-transcriptional assembly of the CF1A/B 3’ processing factor.
DOI: 10.1038/nature09479
发表时间: 2010-12-02
期刊: Nature
影响因子: 64.8
作者:
通讯作者: --
DOI: 10.1016/j.molcel.2008.12.007
发表时间: 2009-01-30
期刊: MOLECULAR CELL
影响因子: 16
作者:
Johnson, Sara Ann;Cubberley, Gabrielle;Bentley, David L.
通讯作者: Bentley, David L.
DOI: 10.1016/j.jmb.2010.06.032
发表时间: 2010-08-20
影响因子: 5.6
作者:
Leeper TC;Qu X;Lu C;Moore C;Varani G
通讯作者: Varani G
DOI: 10.1093/emboj/19.21.5895
发表时间: 2000-11-01
期刊: EMBO JOURNAL
影响因子: 11.4
作者:
de Vries, H;Rüegsegger, U;Keller, W
通讯作者: Keller, W
DOI: 10.1101/gad.11.5.640
发表时间: 1997-03-01
影响因子: 10.5
作者:
Bruhn, L;Munnerlyn, A;Grosschedl, R
通讯作者: Grosschedl, R