An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis. View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Jiao Li, Kaimeng Huang, Gongcheng Hu, Isaac A Babarinde, Yaoyi Li, Xiaotao Dong, Yu-Sheng Chen, Liping Shang, Wenjing Guo, Junwei Wang, Zhaoming Chen, Andrew P Hutchins, Yun-Gui Yang, Hongjie Yao

ABSTRACT

CTCF plays key roles in gene regulation, chromatin insulation, imprinting, X chromosome inactivation and organizing the higher-order chromatin architecture of mammalian genomes. Previous studies have mainly focused on the roles of the canonical CTCF isoform. Here, we explore the functions of an alternatively spliced human CTCF isoform in which exons 3 and 4 are skipped, producing a shorter isoform (CTCF-s). Functionally, we find that CTCF-s competes with the genome binding of canonical CTCF and binds a similar DNA sequence. CTCF-s binding disrupts CTCF/cohesin binding, alters CTCF-mediated chromatin looping and promotes the activation of IFI6 that leads to apoptosis. This effect is caused by an abnormal long-range interaction at the IFI6 enhancer and promoter. Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression. More... »

PAGES

1535

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-019-08949-w

    DOI

    http://dx.doi.org/10.1038/s41467-019-08949-w

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1113184975

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30948729


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