Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Cell Rep. 2018 May 15;23(7):2186-2198. doi: 10.1016/j.celrep.2018.04.039.
The splicing factor SRSF1 promotes nonsense-mediated mRNA decay (NMD), a quality control mechanism that degrades mRNAs with premature termination codons (PTCs). Here we show that transcript-bound SRSF1 increases the binding of NMD factor UPF1 to mRNAs while in, or associated with, the nucleus, bypassing UPF2 recruitment and promoting NMD. SRSF1 promotes NMD when positioned downstream of a PTC, which resembles the mode of action of exon junction complex (EJC) and NMD factors. Moreover, splicing and/or EJC deposition increase the effect of SRSF1 on NMD. Lastly, SRSF1 enhances NMD of PTC-containing endogenous transcripts that result from various events. Our findings reveal an alternative mechanism for UPF1 recruitment, uncovering an additional connection between splicing and NMD. SRSF1's role in the mRNA's journey from splicing to decay has broad implications for gene expression regulation and genetic diseases.
剪接因子 SRSF1 促进无意义介导的 mRNA 降解 (NMD),这是一种质量控制机制,可降解含有提前终止密码子 (PTC) 的 mRNA。在这里,我们表明,与核内或与核内相关的转录本结合的 SRSF1 增加了 NMD 因子 UPF1 与 mRNA 的结合,绕过了 UPF2 的募集并促进了 NMD。当 SRSF1 位于 PTC 的下游时,它会促进 NMD,这类似于外显子结合复合物 (EJC) 和 NMD 因子的作用方式。此外,剪接和/或 EJC 沉积增加了 SRSF1 对 NMD 的影响。最后,SRSF1 增强了由各种事件引起的含有 PTC 的内源性转录本的 NMD。我们的发现揭示了 UPFl 募集的另一种机制,揭示了剪接和 NMD 之间的另一种联系。SRSF1 在 mRNA 从剪接到降解的过程中的作用对基因表达调控和遗传疾病具有广泛的影响。