  Transcriptional repressor CTCF is an important regulator of chromatin 3D
structure, facilitating the formation of topologically associating domains
(TADs). However, its direct effects on gene regulation is less well understood.
Here, we utilize previously published ChIP-seq and RNA-seq data to investigate
the effects of CTCF on alternative splicing of genes with CTCF sites. We
compared the amount of RNA-seq signals in exons upstream and downstream of
binding sites following auxin-induced degradation of CTCF in mouse embryonic
stem cells. We found that changes in gene expression following CTCF depletion
were significant, with a general increase in the presence of upstream exons. We
infer that a possible mechanism by which CTCF binding contributes to
alternative splicing is by causing pauses in the transcription mechanism during
which splicing elements are able to concurrently act on upstream exons already
transcribed into RNA.
