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Transcriptional activators control splicing and 3'-end cleavage levels
Emanuel Rosonina1, Malina A Bakowski, Susan McCracken
1Banting and Best Department of Medical Research and Department of Molecular and Medical Genetics, University of Toronto, Toronto, Ontario M5G 1L6, Canada.
The Journal of Biological Chemistry
|August 27, 2003
Summary
Transcriptional activators enhance constitutive splicing and 3'-end formation. Strong activators boost pre-mRNA processing efficiency independently of transcription levels, revealing a coordinated mechanism.
Area of Science:
- Molecular Biology
- Gene Regulation
- RNA Processing
Background:
- Constitutive splicing and 3 -end formation are crucial steps in pre-mRNA processing.
- The influence of transcriptional activators on these processes beyond transcription levels is not fully understood.
Purpose of the Study:
- To investigate whether transcriptional activators affect the efficiency of constitutive splicing and 3 -end formation.
- To determine if this effect is independent of transcription levels and the mechanism involved.
Main Methods:
- Utilized reporter gene assays to assess splicing and 3 -end cleavage efficiencies.
- Compared the effects of strong versus weak transcriptional activators.
- Investigated the role of the carboxyl-terminal domain of RNA polymerase II.
Main Results:
- Strong transcriptional activators significantly enhance both splicing and 3 -end cleavage efficiencies compared to weak activators.
- The stimulatory effect on pre-mRNA processing is promoter-binding dependent and not solely due to increased transcript levels.
- Activation of splicing and cleavage requires the carboxyl-terminal domain of RNA polymerase II.
- This stimulatory effect was observed across different transcripts and introns.
Conclusions:
- Promoter-bound transcriptional activators play a direct role in enhancing constitutive splicing and 3 -end formation efficiencies.
- These activators coordinate pre-mRNA processing with transcription levels through a mechanism involving RNA polymerase II.