Abstract:
: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.
journal_name
Mol Celljournal_title
Molecular cellauthors
Cramer P,Cáceres JF,Cazalla D,Kadener S,Muro AF,Baralle FE,Kornblihtt ARdoi
10.1016/s1097-2765(00)80372-xsubject
Has Abstractpub_date
1999-08-01 00:00:00pages
251-8issue
2eissn
1097-2765issn
1097-4164pii
S1097-2765(00)80372-Xjournal_volume
4pub_type
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