Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Numerous long intervening noncoding RNAs (lincRNAs) are generated from the mammalian genome by RNA polymerase II (Pol II) transcription. Although multiple functions have been ascribed to lincRNAs, their synthesis and turnover remain poorly characterized. Here, we define systematic differences in transcription and RNA processing between protein-coding and lincRNA genes in human HeLa cells. This is based on a range of nascent transcriptomic approaches applied to different nuclear fractions, including mammalian native elongating transcript sequencing (mNET-seq). Notably, mNET-seq patterns specific for different Pol II CTD phosphorylation states reveal weak co-transcriptional splicing and poly(A) signal-independent Pol II termination of lincRNAs as compared to pre-mRNAs. In addition, lincRNAs are mostly restricted to chromatin, since they are rapidly degraded by the RNA exosome. We also show that a lincRNA-specific co-transcriptional RNA cleavage mechanism acts to induce premature termination. In effect, functional lincRNAs must escape from this targeted nuclear surveillance process.

Original publication

DOI

10.1016/j.molcel.2016.11.029

Type

Journal article

Journal

Mol Cell

Publication Date

05/01/2017

Volume

65

Pages

25 - 38

Keywords

CPSF73, empigen, exosome, lincRNA, mNET-seq, phosphor CTD marks, polyadenylation, splicing, transcription termination, Cell Nucleus, Computational Biology, Databases, Genetic, Exosome Multienzyme Ribonuclease Complex, HeLa Cells, Humans, Phosphorylation, Polyadenylation, RNA Interference, RNA Polymerase II, RNA Precursors, RNA Processing, Post-Transcriptional, RNA Splicing, RNA Stability, RNA, Long Noncoding, RNA, Messenger, Transcription, Genetic, Transfection