Cramer P, Cáceres J F, Cazalla D, Kadener S, Muro A F, Baralle F E, Kornblihtt A R
Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Ciudad Universitaria, Argentina.
Mol Cell. 1999 Aug;4(2):251-8. doi: 10.1016/s1097-2765(00)80372-x.
Alternative mRNA splicing of the fibronectin EDI exon is controlled by a purine-rich exonic splicing enhancer (ESE), postulated as a binding site for SR proteins. By using a transient expression alternative splicing assay combined with promoter swapping, we have demonstrated that the promoter can also control EDI splicing, arguing for coupling between the transcription and splicing machineries. We now report that the SR proteins SF2/ASF and 9G8 stimulate EDI splicing in vivo and that their effect requires an intact EDI ESE. Most importantly, we show that sensitivity to these SR proteins critically depends on the promoter structure, suggesting that the transcription machinery modulates their recruitment to the ESE.
纤连蛋白EDI外显子的可变mRNA剪接受一个富含嘌呤的外显子剪接增强子（ESE）控制，该增强子被假定为SR蛋白的结合位点。通过使用瞬时表达可变剪接分析并结合启动子交换，我们已经证明启动子也可以控制EDI剪接，这表明转录和剪接机制之间存在偶联。我们现在报告说，SR蛋白SF2/ASF和9G8在体内刺激EDI剪接，并且它们的作用需要完整的EDI ESE。最重要的是，我们表明对这些SR蛋白的敏感性关键取决于启动子结构，这表明转录机制调节它们向ESE的募集。
