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Figure 4. KDM2B ZF-CxxC DNA binding domain is required for CGI binding.(A) Schematic representation showing removal of RING1B in ESC Ring1a−/− Ring1bfl/fl cells by tamoxifen treatment. (B) ChIP analysis indicating that RING1B is enriched at polycomb target CGIs in untreated cells (red bars). After 48 hr of tamoxifen treatment RING1B binding is lost at polycomb targets (blue bars). Error bars represent SEM of three biological replicates. (C) ChIP analysis demonstrating that removal of RING1B does not lead to loss of KDM2B binding at regular or polycomb associated target CGIs (compare red and green bars). This demonstrates that RING1B is not required to recruit KDM2B to polycomb repressed sites. Error bars represent SEM of three biological replicates. (D) ChIP analysis in ESC cells stably expressing tagged wild-type (WT) KDM2B or a mutant KDM2B that disrupts its DNA-binding capacity (K643A).The ZF-CxxC domain of KDM2B is required for KDM2B binding to CGIs regardless of their polycomb status. Error bars represent SEM of two biological replicates.DOI: http://dx.doi.org/10.7554/eLife.00205.009 Image published in: Farcas AM et al. (2012) Copyright © 2012, Farcas et al. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution license Larger Image Printer Friendly View

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