한빛사 논문
Christopher C. Venters1, Jung-Min Oh1, Chao Di, Byung Ran So and Gideon Dreyfuss*
Howard Hughes Medical Institute, Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104
1 These authors contributed equally to this work.
*Correspondence : Gideon Dreyfuss
Abstract
Recent observations showed that nascent RNA polymerase II transcripts, pre-mRNAs, and noncoding RNAs are highly susceptible to premature 3′-end cleavage and polyadenylation (PCPA) from numerous intronic cryptic polyadenylation signals (PASs). The importance of this in gene regulation was not previously appreciated as PASs, despite their prevalence, were thought to be active in terminal exons at gene ends. Unexpectedly, antisense oligonucleotide interference with U1 snRNA base-pairing to 5′ splice sites, which is necessary for U1 snRNP’s (U1) function in splicing, caused widespread PCPA in metazoans. This uncovered U1’s PCPA suppression activity, termed telescripting, as crucial for full-length transcription in thousands of vertebrate genes, providing a general role in transcription elongation control. Progressive intron-size expansion in metazoan evolution greatly increased PCPA vulnerability and dependence on U1 telescripting. We describe how these observations unfolded and discuss U1 telescripting’s role in shaping the transcriptome.
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