DNA damage induces apoptosis and many apoptotic genes are regulated via 
alternative splicing (AS), but little is known about the control mechanisms. 
Here we show that ultraviolet irradiation (UV) affects cotranscriptional AS in a 
p53-independent way, through the hyperphosphorylation of RNA polymerase II 
carboxy-terminal domain (CTD) and a subsequent inhibition of transcriptional 
elongation, estimated in vivo and in real time. Phosphomimetic CTD mutants not 
only display lower elongation but also duplicate the UV effect on AS. 
Consistently, nonphosphorylatable mutants prevent the UV effect. Apoptosis 
promoted by UV in cells lacking p53 is prevented when the change in AS of the 
apoptotic gene bcl-x is reverted, confirming the relevance of this mechanism. 
Splicing-sensitive microarrays revealed a significant overlap of the subsets of 
genes that have changed AS with UV and those that have reduced expression, 
suggesting that transcriptional coupling to AS is a key feature of the 
DNA-damage response.