BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites.

ABSTRACT:

Background

Pervasive usage of alternative promoters leads to the deregulation of gene expression in carcinogenesis and may drive the emergence of new genes in spermatogenesis. However, little is known regarding the mechanisms underpinning the activation of alternative promoters.

Results

Here we describe how alternative cancer-testis-specific transcription is activated. We show that intergenic and intronic CTCF binding sites, which are transcriptionally inert in normal somatic cells, could be epigenetically reprogrammed into active de novo promoters in germ and cancer cells. BORIS/CTCFL, the testis-specific paralog of the ubiquitously expressed CTCF, triggers the epigenetic reprogramming of CTCF sites into units of active transcription. BORIS binding initiates the recruitment

SUBMITTER: Pugacheva EM 

PROVIDER: S-EPMC10832218 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature