Department of Biochemistry and Biophysics, School of Medicine and Dentistry, University of Rochester, Rochester, New York 14642, USA.
Genes Dev. 2013 Apr 1;27(7):793-804. doi: 10.1101/gad.212639.112. Epub 2013 Apr 4.
Staufen1-mediated mRNA decay (SMD) degrades mRNAs that harbor a Staufen1-binding site (SBS) in their 3' untranslated regions (UTRs). Human SBSs can form by intermolecular base-pairing between a 3' UTR Alu element and an Alu element within a long noncoding RNA (lncRNA) called a ½-sbsRNA. Since Alu elements are confined to primates, it was unclear how SMD occurs in rodents. Here we identify mouse mRNA 3' UTRs and lncRNAs that contain a B1, B2, B4, or identifier (ID) element. We show that SMD occurs in mouse cells via mRNA-lncRNA base-pairing of partially complementary elements and that mouse ½-sbsRNA (m½-sbsRNA)-triggered SMD regulates C2C12 cell myogenesis. Our findings define new roles for lncRNAs as well as B and ID short interspersed elements (SINEs) in mice that undoubtedly influence many developmental and homeostatic pathways.
Staufen1 介导的 mRNA 降解（SMD）降解在其 3'非翻译区（UTR）中含有 Staufen1 结合位点（SBS）的 mRNAs。人类 SBS 可以通过 3'UTR Alu 元件和称为½-sbsRNA 的长非编码 RNA（lncRNA）内的 Alu 元件之间的分子间碱基配对形成。由于 Alu 元件仅限于灵长类动物，因此尚不清楚 SMD 如何在啮齿动物中发生。在这里，我们鉴定了含有 B1、B2、B4 或标识符（ID）元件的小鼠 mRNA 3'UTR 和 lncRNA。我们表明，SMD 通过部分互补元件的 mRNA-lncRNA 碱基配对在小鼠细胞中发生，并且小鼠½-sbsRNA（m½-sbsRNA）触发的 SMD 调节 C2C12 细胞肌发生。我们的发现为 lncRNA 以及 B 和 ID 短散布元件（SINE）在小鼠中的新作用提供了依据，这无疑会影响许多发育和动态平衡途径。
