Journal
RNA
Volume 19, Issue 1, Pages 96-102Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1261/rna.037044.112
Keywords
SR protein; hnRNP protein; pre-mRNA splicing; splicing activation; splicing repression
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Funding
- Stiftung fur AIDS-Forschung, Dusseldorf
- Jurgen-Manchot-Stiftung
- Boehringer Ingelheim Fonds
- NIH [RO1 GM62287, R21 CA149548]
- German Academic Exchange Service, DAAD
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Alternative splicing is regulated by splicing factors that modulate splice site selection. In some cases, however, splicing factors show antagonistic activities by either activating or repressing splicing. Here, we show that these opposing outcomes are based on their binding location relative to regulated 5' splice sites. SR proteins enhance splicing only when they are recruited to the exon. However, they interfere with splicing by simply relocating them to the opposite intronic side of the splice site. hnRNP splicing factors display analogous opposing activities, but in a reversed position dependence. Activation by SR or hnRNP proteins increases splice site recognition at the earliest steps of exon definition, whereas splicing repression promotes the assembly of nonproductive complexes that arrest spliceosome assembly prior to splice site pairing. Thus, SR and hnRNP splicing factors exploit similar mechanisms to positively or negatively influence splice site selection.
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