Dirksen W P, Hampson R K, Sun Q, Rottman F M
Department of Molecular Biology and Microbiology, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4960.
J Biol Chem. 1994 Mar 4;269(9):6431-6.
A previous study has demonstrated that deletion of a region within the last exon of bovine growth hormone (bGH) pre-mRNA results in almost complete retention of the upstream intron (Hampson, R. K., LaFollette, L., and Rottman, F. M. (1989) Mol. Cell. Biol. 9, 1604-1610). We now demonstrate that insertion of a simple purine-rich element (GGAAG), which is present within the deleted region, activates intron splicing upon expression in transfected cells. Moreover, several repeats of the GGAA(G) sequence restore splicing to near wild-type levels and direct the binding of a factor present in HeLa cell nuclear extracts. Mutation of the 5'-splice site toward U1 small nuclear RNA complementarity eliminates dependence on the downstream exon sequence for splicing. These results support a model for alternative intron retention in which purine-rich sequences function as part of an "exonic splicing enhancer" to complement a weak 5'-splice site and thereby facilitate intron removal. As a result, the majority of bGH mRNA is processed to remove intron D while still allowing a fraction of bGH mRNA containing the intact intron to reach the cytoplasm.
先前的一项研究表明,牛生长激素(bGH)前体mRNA最后一个外显子内一个区域的缺失导致上游内含子几乎完全保留(汉普森,R.K.,拉福莱特,L.,和罗特曼,F.M.(1989年)《分子与细胞生物学》9,1604 - 1610)。我们现在证明,在缺失区域内存在的一个简单的富含嘌呤的元件(GGAAG)的插入,在转染细胞中表达时可激活内含子剪接。此外,GGAA(G)序列的几个重复将剪接恢复到接近野生型水平,并指导HeLa细胞核提取物中一种因子的结合。5'-剪接位点向U1小核RNA互补性的突变消除了剪接对下游外显子序列的依赖性。这些结果支持了一种选择性内含子保留模型,其中富含嘌呤的序列作为“外显子剪接增强子”的一部分发挥作用,以补充弱的5'-剪接位点,从而促进内含子的去除。结果,大多数bGH mRNA被加工以去除内含子D,同时仍允许一小部分含有完整内含子的bGH mRNA到达细胞质。