通用剪接因子SF2/ASF通过与外显子剪接增强子结合来促进可变剪接。

General splicing factor SF2/ASF promotes alternative splicing by binding to an exonic splicing enhancer.

作者信息

Sun Q, Mayeda A, Hampson R K, Krainer A R, Rottman F M

机构信息

Department of Molecular Biology and Microbiology, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4960.

出版信息

Genes Dev. 1993 Dec;7(12B):2598-608. doi: 10.1101/gad.7.12b.2598.

DOI:10.1101/gad.7.12b.2598

PMID:8276242

Abstract

The general splicing factor SF2/ASF binds in a sequence-specific manner to a purine-rich exonic splicing enhancer (ESE) in the last exon of bovine growth hormone (bGH) pre-mRNA. More importantly, SF2/ASF stimulates in vitro splicing of bGH intron D through specific interaction with the ESE sequences. However, another general splicing factor, SC35, does not bind the ESE sequences and has no effect on bGH intron D splicing. Thus, one possible function of SF2/ASF in alternative and, perhaps, constitutive pre-mRNA splicing is to recognize ESE sequences. The stimulation of bGH intron D splicing by SF2/ASF is counteracted by the addition of hnRNP A1. The relative levels of SF2/ASF and hnRNP A1 influence the efficiency of bGH intron D splicing in vitro and may be the underlying mechanism of this alternative pre-mRNA processing event in vivo.

摘要

通用剪接因子SF2/ASF以序列特异性方式与牛生长激素（bGH）前体mRNA最后一个外显子中的富含嘌呤的外显子剪接增强子（ESE）结合。更重要的是，SF2/ASF通过与ESE序列的特异性相互作用刺激bGH内含子D的体外剪接。然而，另一种通用剪接因子SC35不结合ESE序列，对bGH内含子D剪接没有影响。因此，SF2/ASF在可变剪接以及可能的组成型前体mRNA剪接中的一个可能功能是识别ESE序列。添加hnRNP A1可抵消SF2/ASF对bGH内含子D剪接的刺激作用。SF2/ASF和hnRNP A1的相对水平影响bGH内含子D体外剪接的效率，可能是体内这种可变前体mRNA加工事件的潜在机制。