Department of Anatomy, Kansai Medical University, Hirakata, Osaka, 573-1010, Japan.
Department of Anatomy, Kansai Medical University, Hirakata, Osaka, 573-1010, Japan.
Biochem Biophys Res Commun. 2021 Jan 1;534:491-497. doi: 10.1016/j.bbrc.2020.11.054. Epub 2020 Nov 19.
Cytoplasmic polyadenylation element binding protein 1 (CPEB1) regulates polyadenylation and subsequent translation of CPE-containing mRNAs involved in various physiological and pathological phenomena. Although the significance of CPEB1-mediated translational regulation has recently been reported, the detailed regulatory mechanism of Cpeb1 expression remains unclear. To elucidate the post-transcriptional regulatory mechanisms of Cpeb1 expression, we constructed reporter plasmids containing various deletions or mutations in the Cpeb1 mRNA 3' untranslated region (3'UTR). We investigated their expression levels in Neuro2a neuroblastoma cells. We found that Cpeb1 expression is regulated through an AU-rich element in its 3'UTR. Furthermore, the mRNA decay factor AU-rich binding factor 1 (AUF1) regulates Cpeb1 expression, and knockdown of AUF1 upregulates Cpeb1 mRNA expression but results in a decrease in CPEB1 protein levels. These findings indicate that AUF1 has a discordant role in the expression of Cpeb1.
细胞质多聚腺苷酸化元件结合蛋白 1(CPEB1)调节多聚腺苷酸化,并随后翻译参与各种生理和病理现象的含有 CPE 的 mRNA。尽管 CPEB1 介导的翻译调控的意义最近已经被报道,但是 Cpeb1 表达的详细调控机制仍然不清楚。为了阐明 Cpeb1 表达的转录后调控机制,我们构建了含有 Cpeb1 mRNA 3'非翻译区(3'UTR)中各种缺失或突变的报告质粒。我们在 Neuro2a 神经母细胞瘤细胞中研究了它们的表达水平。我们发现 Cpeb1 的表达受其 3'UTR 中的 AU 丰富元件调节。此外,mRNA 衰变因子 AU 丰富结合因子 1(AUF1)调节 Cpeb1 的表达,并且 AUF1 的敲低会上调 Cpeb1 mRNA 的表达,但会导致 CPEB1 蛋白水平降低。这些发现表明 AUF1 在 Cpeb1 的表达中具有不一致的作用。