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. 2016 Feb 16;73(9):1871–1879. doi: 10.1007/s00018-016-2157-6

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© The Author(s) 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 6 — The ATRX/Daxx/H3.3 complex continuously maintain heterochromatin at imprinted DMRs. ATRX can directly bind H3K9me3 at imprinted DMRs to recruit Daxx and deposit the replication-independent H3.3 histone variant. Daxx interacts with the KAP1 co-repressor complex which recruits Setdb1 to catalyse H3K9me3 heterochromatin at these sites. The replication-independent nature of H3.3 ensures the continuous maintenance of heterochromatin at gDMRs throughout the cell cycle particularly during transcription