Fig. 6

Graphic representations of the RNAPII NET-seq results at (a) AKAP and (b) CAPER. RNAPII localization signals normalized as NET-seq read count signals. Blue arrows indicate the position the final nucleotide added by RNAPII, while green arrow indicates the movement of the polymerase (c). ‘Kinetic model’ of PARP1–chromatin binding effects on RNAPII elongation, with consequences in alternative splicing regulation. PARP1 creates and/or maintains a chromatin structure, which is poised for transcription elongation. This structure enables RNAPII to pause, allowing enough resident time for RNAPII and its associated splicing factors to recognize specific splice sites, resulting in exon inclusion. In the absence of PARP1, the poised state is resolved to a more active chromatin structure, thus no pausing of the fast RNAPII, resulting in exon skipping. Although this model can explain our results of lengthening of the transcripts after PARP1 knockdown, it does not explain shortening of transcripts after knockdown