A slow RNA polymerase II affects alternative splicing in vivo.

By M. L. de la Mata, C. Alonso, Sebastian Kadener, J. P. Fededa, M. Blaustein, Federico Pelisch, P. Cramer, D. Bentley, A. Kornblihtt. Molecules and Cells, 2003

755 citations recorded by the source corpus.

Subfields: Political Science and International Relations, Sociology and Political Science

View Paper: https://www.semanticscholar.org/paper/f6671a1844b2e649fc98d417b1b739f18aa6e514

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Citations in the corpus

Elongation by RNA polymerase II: the short and long of it. (2004, background): “Fascinatingly, an RNA polymerase with a slow elongation rate gave rise to different outcomes with respect to alternative splicing, implying that elongation events control splice-site selection (de la Mata et al. 2003).”
CTCF-promoted RNA polymerase II pausing links DNA methylation to splicing (2011, positive): “and (2) the rate of RNA polymerase II (pol II) transcription elongation, wherein a slow rate favours co-transcriptional spliceosome assembly at weak splice site”
Deep sequencing of subcellular RNA fractions shows splicing to be predominantly co-transcriptional in the human genome but inefficient for lncRNAs (2012, background): “…constitute well-studied examples of co-transcriptional splicing—the fibronectin (Cramer et al. 1997; Kadener et al. 2001; Nogues et al. 2002; de la Mata et al. 2003; reads from the total chromatin fraction and excluding all exons that are within 250 bp of a potential novel splice site, we…”
Past, present, and future of circRNAs (2019, positive): “This could be achieved by modulation of trans-acting splicing factors or by changes in the kinetics of RNA polymerase II transcription, which are known to modulate alternative splicing (Kadener et al , 2001, 2002; de la Mata et al , 2003).”
Splicing regulation: from a parts list of regulatory elements to an integrated splicing code. (2008, background): “For example, a mutated RNA polymerase II with a slow elongation rate had been shown to affect the AS of endogenous genes (de la Mata et al. 2003), and the insertion of a transcription-pausing element, MAZ4, into a minigene construct can influence splicing of an alternative exon (Robson-Dixon and…”
Differential chromatin marking of introns and expressed exons by H3K36me3 (2009, background): “It is also known that the rate of RNA polymerase procession can vary over the gene and that changes in processivity can affect inclusion of alternative exon”
Ending the message: poly(A) signals then and now. (2011, background): “…well known that Pol II processivity set up by specific promoters, by modification of Pol II activity (such as UV-induced hyperphosphorylation of CTD), or by use of an artificial mutant (so-called slow Pol II) can influence alternative splicing patterns (de la Mata et al. 2003; Munoz et al. 2009).”
Understanding the language of Lys36 methylation at histone H3 (2012, neutral): “melanogaster results in different inclusion patterns of the exons within the Ultrabithorax mRN”
Mechanisms of alternative splicing regulation: insights from molecular and genomics approaches (2009, methodology): “In support of this model, an RNAP II with a reduced elongation rate caused by a point mutation was found to greatly stimulate the inclusion of an alternative exon that has weak splice site”
Epigenetics in alternative pre-mRNA splicing (2011, positive): “The strongest evidence for a kinetic role of RNA Pol II elongation comes, however, from a slow mutant of RNA Pol II, which increases E33 inclusion in human cells (de la Mata et al., 2003).”