剪接是通过将被称为“内含子”的RNA片段除掉来从大前体分子(pre-mRNA)生成信使RNA (mRNA)的过程，该过程由被称为snRNP的“蛋白-RNA复合物”完成。一个剪接体含有相同数量的U1、 U2、U4、U5和U6 snRNP，但U1 snRNP水平远远超过剪接体所需水平，从而导致这样的观点：“多余”的U1也许有独立于剪接的功能。现在，一个这样的功能已被发现，它涉及U1 snRNA和一些pre-mRNA之间的相互作用，后者含有带“多腺苷酸化”点的“内含子”。这可通过防止过早终止及“多腺苷酸化”来保护新生成的pre-mRNA不受损伤。（生物谷Bioon.com）
生物谷推荐原文出处：
Nature doi:10.1038/nature09479
U1 snRNP protects pre-mRNAs from premature cleavage and polyadenylation
Daisuke Kaida1, Michael G. Berg1, Ihab Younis1, Mumtaz Kasim1, Larry N. Singh1, Lili Wan1 & Gideon Dreyfuss1
Howard Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6148, USA
Correspondence to: Gideon Dreyfuss1 Email: gdreyfuss@hhmi.upenn.edu
Top of pageAbstractIn eukaryotes, U1 small nuclear ribonucleoprotein (snRNP) forms spliceosomes in equal stoichiometry with U2, U4, U5 and U6 snRNPs; however, its abundance in human far exceeds that of the other snRNPs. Here we used antisense morpholino oligonucleotide to U1 snRNA to achieve functional U1 snRNP knockdown in HeLa cells, and identified accumulated unspliced pre-mRNAs by genomic tiling microarrays. In addition to inhibiting splicing, U1 snRNP knockdown caused premature cleavage and polyadenylation in numerous pre-mRNAs at cryptic polyadenylation signals, frequently in introns near (<5?kilobases) the start of the transcript. This did not occur when splicing was inhibited with U2 snRNA antisense morpholino oligonucleotide or the U2-snRNP-inactivating drug spliceostatin A unless U1 antisense morpholino oligonucleotide was also included. We further show that U1 snRNA–pre-mRNA base pairing was required to suppress premature cleavage and polyadenylation from nearby cryptic polyadenylation signals located in introns. These findings reveal a critical splicing-independent function for U1 snRNP in protecting the transcriptome, which we propose explains its overabundance.
