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. 2014 Oct;24(10):1584–1594. doi: 10.1101/gr.173831.114

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© 2014 Ivanauskiene et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Model of regulation of loading of H3.3 on chromatin by DEK. (A) Outside telomeres, DEK prevents chromatin loading of nonnucleosomal H3.3, which is recruited to PML NBs by DAXX (Delbarre et al. 2013). Loss of DEK by siRNA relaxes DNA topology and promotes broad HIRA-dependent H3.3 deposition on chromosome arms (lower right) and DAXX/ATRX-dependent loading in H3K9me3- and CBX3-containing heterochromatin foci where PML NBs also aggregate (upper right). (B) At telomeres, DEK has been previously shown to be essential for anchoring of PML NBs and ATRX, enabling H3.3 loading, and this is required to preserve telomere chromatin integrity (Chang et al. 2013). Loss of DEK results in dislocation of PML NBs and ATRX, impairment of H3.3 loading, and a fragile telomere phenotype marked by TERF1 spreading, telomere elongation, and up-regulation of the TERRA long noncoding RNA. The mislocated PML/ATRX/H3.3 complex may be relocated to pericentric heterochromatin.