Nishioka Kenichi, Wang Xian-Feng, Miyazaki Hitomi, Soejima Hidenobu, Hirose Susumu
Division of Molecular Genetics and Epigenetics, Department of Biomolecular Sciences, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga City, Saga 849-8501, Japan
Division of Gene Expression, Department of Developmental Genetics, National Institute of Genetics, 1111 Yata, Mishima City, Shizuoka 411-8540, Japan.
Development. 2018 Mar 9;145(5):dev162461. doi: 10.1242/dev.162461.
Under stress conditions, the coactivator Multiprotein bridging factor 1 (Mbf1) translocates from the cytoplasm into the nucleus to induce stress-response genes. However, its role in the cytoplasm, where it is mainly located, has remained elusive. Here, we show that Mbf1 associates with mRNA and protects it from degradation by the exoribonuclease Pacman (Pcm), thereby ensuring Polycomb silencing. In genetic studies, loss of function enhanced a Polycomb phenotype in Polycomb group mutants, and was accompanied by a significant reduction in mRNA expression. Furthermore, a mutation suppressed the Polycomb phenotype and restored the expression level of mRNA, while overexpression exhibited the Polycomb phenotype in the mutant but not in the wild-type background. , Mbf1 protected RNA from Pcm activity. Our results suggest that Mbf1 buffers fluctuations in Pcm activity to maintain an mRNA expression level sufficient for Polycomb silencing.
在应激条件下，共激活因子多蛋白桥接因子1（Mbf1）从细胞质转移到细胞核，以诱导应激反应基因。然而，它在主要定位的细胞质中的作用仍然难以捉摸。在这里，我们表明Mbf1与mRNA结合，并保护其免受外切核糖核酸酶Pacman（Pcm）的降解，从而确保多梳沉默。在遗传学研究中，功能丧失增强了多梳组突变体中的多梳表型，并伴随着mRNA表达的显著降低。此外，一个突变抑制了多梳表型并恢复了mRNA的表达水平，而过表达在突变体中表现出多梳表型，但在野生型背景中则没有。Mbf1保护RNA免受Pcm活性的影响。我们的结果表明，Mbf1缓冲Pcm活性的波动，以维持足以进行多梳沉默的mRNA表达水平。
