Yamada Hiroko, Horigome Chihiro, Okada Takafumi, Shirai Chiharu, Mizuta Keiko
Department of Biofunctional Science and Technology, Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Japan.
RNA. 2007 Nov;13(11):1977-87. doi: 10.1261/rna.553807. Epub 2007 Sep 5.
We previously cloned RRP14/YKL082c, whose product exhibits two-hybrid interaction with Ebp2p, a regulatory factor of assembly of 60S ribosomal subunits. Depletion of Rrp14p results in shortage of 60S ribosomal subunits and retardation of processing from 27S pre-rRNA to 25S rRNA. Furthermore, 35S pre-rRNA synthesis appears to decline in Rrp14p-depleted cells. Rrp14p interacts with regulatory factors of 60S subunit assembly and also with Utp11p and Faf1p, which are regulatory factors required for assembly of 40S ribosomal subunits. We propose that Rrp14p is involved in ribosome synthesis from the beginning of 35S pre-rRNA synthesis to assembly of the 60S ribosomal subunit. Disruption of RRP14 causes an extremely slow growth rate of the cell, a severe defect in ribosome synthesis, and a depolarized localization of cortical actin patches throughout the cell cycle. These results suggest that Rrp14p has dual functions in ribosome synthesis and polarized cell growth.
我们之前克隆了RRP14/YKL082c，其产物与Ebp2p存在双杂交相互作用，Ebp2p是60S核糖体亚基组装的调节因子。Rrp14p的缺失会导致60S核糖体亚基短缺，并阻碍从27S前体rRNA到25S rRNA的加工。此外，在Rrp14p缺失的细胞中，35S前体rRNA的合成似乎会减少。Rrp14p与60S亚基组装的调节因子相互作用，还与Utp11p和Faf1p相互作用，Utp11p和Faf1p是40S核糖体亚基组装所需的调节因子。我们提出，Rrp14p从35S前体rRNA合成开始到60S核糖体亚基的组装都参与核糖体合成。RRP14的破坏导致细胞生长速度极慢、核糖体合成严重缺陷以及在整个细胞周期中皮质肌动蛋白斑的定位去极化。这些结果表明，Rrp14p在核糖体合成和极化细胞生长中具有双重功能。
