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Access through your institution Buy or subscribe The authors observed changes in AS patterns in various genes, including the pro-apoptotic _BCLX_ gene, in UV-irradiated cells. Similar
effects on AS were seen with another DNA-damaging agent, which together suggest that AS is affected by DNA damage. Given that the tumour suppressor p53 is an important regulator of the
cellular response to DNA damage, it was somewhat surprising to find UV-induced changes in AS in p53 null cells; the effect is therefore independent of p53. Splicing can occur both
co-transcriptionally and post-transcriptionally, but the effect of UV on AS is strictly co-transcriptional. This led the authors to investigate the effects of UV irradiation on RNA
polymerase II-mediated transcription and, specifically, on its CTD, which is hyperphosphorylated in response to UV. Indeed, changes in AS occur after hyperphosphorylation of the CTD, and
non-irradiated cells expressing a phosphomimetic CTD mutant duplicate the effect of UV on AS. By contrast, non-phosphorylatable CTD mutants or chemical inhibition of UV-dependent CTD
phosphorylation prevent the UV effect on AS. Together, these findings suggest a causal relationship between CTD hyperphosphorylation and a change in AS. This is a preview of subscription
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ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support ORIGINAL RESEARCH PAPER * Muñoz, M. J. et al. DNA damage regulates alternative
splicing through inhibition of RNA polymerase II elongation. _Cell_ 137, 708–720 (2009) Article Google Scholar Download references Authors * Arianne Heinrichs View author publications You
can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Heinrichs, A. UV-induced coupling. _Nat Rev Mol
Cell Biol_ 10, 440 (2009). https://doi.org/10.1038/nrm2715 Download citation * Published: 03 June 2009 * Issue Date: July 2009 * DOI: https://doi.org/10.1038/nrm2715 SHARE THIS ARTICLE
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