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. 2016 Oct 24;45(3):1114–1129. doi: 10.1093/nar/gkw979

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© The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Model for KDM2A-mediated establishment of heterochromatin. The CXXC-Znf enables KDM2A to bind chromatin containing no pre-existing DNA and histone modifications (top). Binding of HP1 to the KDM2A LTVTL motif establishes an alternative to the HP1 recruitment mechanism via the H3K9me3-modification deposited by H3K9 lysine methyltransferases (KMTs) that does not require the K3K9me3 mark. Subsequent deposition of the H3K9me3-modification by H3K9 KMTs leads to reinforced HP1 binding and a stabilization of the KDM2A/HP1/nucleosome interaction. The ability of HP1 to recruit DNMTs leads to deposition of CpG methylation (black pinheads) which results in loss of KDM2A leaving behind DNA-methylated, H3K9me3-modified and HP1-decorated heterochromatin (bottom).