Abstract:
:While intron retention (IR) is considered a widely conserved and distinct mechanism of gene expression control, its regulation is poorly understood. Here we show that DNA methylation directly regulates IR. We also find reduced occupancy of MeCP2 near the splice junctions of retained introns, mirroring the reduced DNA methylation at these sites. Accordingly, MeCP2 depletion in tissues and cells enhances IR. By analysing the MeCP2 interactome using mass spectrometry and RNA co-precipitation, we demonstrate that decreased MeCP2 binding near splice junctions facilitates IR via reduced recruitment of splicing factors, including Tra2b, and increased RNA polymerase II stalling. These results suggest an association between IR and a slower rate of transcription elongation, which reflects inefficient splicing factor recruitment. In summary, our results reinforce the interdependency between alternative splicing involving IR and epigenetic controls of gene expression.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Wong JJ,Gao D,Nguyen TV,Kwok CT,van Geldermalsen M,Middleton R,Pinello N,Thoeng A,Nagarajah R,Holst J,Ritchie W,Rasko JEJdoi
10.1038/ncomms15134subject
Has Abstractpub_date
2017-05-08 00:00:00pages
15134issn
2041-1723pii
ncomms15134journal_volume
8pub_type
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