Pan Qun, Saltzman Arneet L, Kim Yoon Ki, Misquitta Christine, Shai Ofer, Maquat Lynne E, Frey Brendan J, Blencowe Benjamin J
Banting and Best Department of Medical Research, University of Toronto, Ontario, M5G 1L6, Canada.
Genes Dev. 2006 Jan 15;20(2):153-8. doi: 10.1101/gad.1382806.
Sequence-based analyses have predicted that approximately 35% of mammalian alternative splicing (AS) events produce premature termination codon (PTC)-containing splice variants that are targeted by the process of nonsense-mediated mRNA decay (NMD). This led to speculation that AS may often regulate gene expression by activating NMD. Using AS microarrays, we show that PTC-containing splice variants are generally produced at uniformly low levels across diverse mammalian cells and tissues, independently of the action of NMD. Our results suggest that most PTC-introducing AS events are not under positive selection pressure and therefore may not contribute important functional roles.
基于序列的分析预测，大约35%的哺乳动物可变剪接（AS）事件会产生含过早终止密码子（PTC）的剪接变体，这些变体可被无义介导的mRNA降解（NMD）过程靶向识别。这引发了一种推测，即可变剪接可能经常通过激活NMD来调节基因表达。使用AS微阵列，我们发现含PTC的剪接变体在各种哺乳动物细胞和组织中通常以统一的低水平产生，与NMD的作用无关。我们的结果表明，大多数引入PTC的可变剪接事件并不处于正选择压力之下，因此可能不具有重要的功能作用。
