Wakatsuki Shuji, Araki Toshiyuki
Department of Peripheral Nervous System Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Front Mol Neurosci. 2021 Sep 24;14:748721. doi: 10.3389/fnmol.2021.748721. eCollection 2021.
Small non-coding vault RNAs (vtRNAs) have been described as a component of the vault complex, a hollow-and-barrel-shaped ribonucleoprotein complex found in most eukaryotes. It has been suggested that the function of vtRNAs might not be limited to simply maintaining the structure of the vault complex. Despite the increasing research on vtRNAs, little is known about their physiological functions. Recently, we have shown that murine vtRNA (mvtRNA) up-regulates synaptogenesis by activating the mitogen activated protein kinase (MAPK) signaling pathway. mvtRNA binds to and activates mitogen activated protein kinase 1 (MEK1), and thereby enhances MEK1-mediated extracellular signal-regulated kinase activation. Here, we introduce the regulatory mechanism of MAPK signaling in synaptogenesis by vtRNAs and discuss the possibility as a novel molecular basis for synapse formation.
小型非编码穹窿RNA（vtRNA）被认为是穹窿复合体的一个组成部分，穹窿复合体是一种存在于大多数真核生物中的中空桶状核糖核蛋白复合体。有人提出，vtRNA的功能可能不仅限于简单维持穹窿复合体的结构。尽管对vtRNA的研究日益增多，但其生理功能仍知之甚少。最近，我们发现小鼠vtRNA（mvtRNA）通过激活丝裂原活化蛋白激酶（MAPK）信号通路来上调突触形成。mvtRNA与丝裂原活化蛋白激酶1（MEK1）结合并激活它，从而增强MEK1介导的细胞外信号调节激酶的激活。在此，我们介绍vtRNA在突触形成中对MAPK信号的调控机制，并探讨其作为突触形成新分子基础的可能性。
