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The competition between splicing and 3' processing shapes the human transcriptome.

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    Disrupting pre-mRNA splicing activates thousands of intronic polyadenylation sites and causes premature transcription termination. Conversely, inhibiting 3' processing globally enhances splicing, revealing a competitive interplay shaping the transcriptome.

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    Area of Science:

    • Molecular Biology
    • Gene Regulation
    • Transcriptional Control

    Background:

    • Eukaryotic pre-mRNA processing involves coordinated splicing and 3' processing.
    • The precise mechanisms governing this coordination, particularly the role of U1 snRNP in inhibiting 3' processing (telescripting), are not fully understood.

    Purpose of the Study:

    • To investigate the interplay between splicing and 3' processing.
    • To elucidate the mechanisms by which splicing factors influence 3' processing and transcription termination.

    Main Methods:

    • Targeting key splicing factors (U1 snRNP, U2 snRNP, U2AF, SF3b) to disrupt splicing.
    • Analyzing the activation of intronic polyadenylation (IPA) sites.
    • Assessing premature transcription termination within gene bodies.
    • Inhibiting 3' processing to observe effects on splicing.

    Main Results:

    • Splicing disruption, particularly of U1 snRNP, activated thousands of IPA sites.
    • Splicing inhibition led to widespread premature transcription termination via IPA-coupled and independent pathways.
    • Different splicing factors differentially regulated IPA sites.
    • Inhibition of 3' processing globally enhanced splicing.

    Conclusions:

    • Splicing and 3' processing are competing processes.
    • These processes intersect with transcription to regulate gene expression.
    • The findings challenge the telescripting model and propose a broader regulatory network.