Abstract:
:Although DNA methylation is commonly invoked as a mechanism for transcriptional repression, the extent to which it actively silences transcription factor (TF) occupancy sites in vivo is unknown. To study the role of DNA methylation in the active modulation of TF binding, we quantified the effect of DNA methylation depletion on the genomic occupancy patterns of CTCF, an abundant TF with known methylation sensitivity that is capable of autonomous binding to its target sites in chromatin. Here, we show that the vast majority (>98.5%) of the tens of thousands of unoccupied, methylated CTCF recognition sequences remain unbound upon abrogation of DNA methylation. The small fraction of sites that show methylation-dependent binding in vivo are in turn characterized by highly variable CTCF occupancy across cell types. Our results suggest that DNA methylation is not a primary groundskeeper of genomic TF landscapes, but rather a specialized mechanism for stabilizing intrinsically labile sites.
journal_name
Cell Repjournal_title
Cell reportsauthors
Maurano MT,Wang H,John S,Shafer A,Canfield T,Lee K,Stamatoyannopoulos JAdoi
10.1016/j.celrep.2015.07.024subject
Has Abstractpub_date
2015-08-18 00:00:00pages
1184-95issue
7issn
2211-1247pii
S2211-1247(15)00764-0journal_volume
12pub_type
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