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. 2024 Jul 29;17:1446686. doi: 10.3389/fnmol.2024.1446686

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Copyright © 2024 van der Laan, ten Voorde, Mannens and Henneman.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Thyroid Hormone Receptor Interactor 12 (TRIP12) mediates the maintenances of a repressive ubiquitin signal added by the Polycomb Repressive Complex (PRC). PRC mediated DNA methylation on adenine position 6 (6 mA) results in TRIP12 polyubiquitination of Additional Sex Combs Like 1 (ASXL1), which is a subunit from the Polycomb Repressive Deubiquitinase (PR-DUB) complex. This leads to the proteasomal degradation of PR-DUB and therefore the maintenance of the ubiquitin marks added by PRC1. If no 6 mA is present on PRC repressed genes, there is also no TRIP12 present. This means ASXL1 can target PR-DUB to H2AK119 monoubiquitination. This leads of the deubiquitination of that histone by BRCA1 Associated Protein 1 (BAP1) and therefore a loss of the repressive mark (Created with BioRender).