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. 2019 Apr;29(4):564–575. doi: 10.1101/gr.239277.118

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© 2019 Rasmussen 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 1. — TET2 chromatin immunoprecipitation and sequencing on wild-type and epitope-tagged cell lines. (A) Representative ChIP-seq tracks of either V5 (left) or 2xFL (right) ChIP experiments in ES cells using different crosslinking conditions. (FA) formaldehyde; (DSG) disuccinimidyl glutarate; (EGS) ethylene glycol bis(succinimidyl succinate). (B) Histograms showing the number of called peaks in the different crosslinking conditions in V5-TET2 (upper) or 2xFL-TET2 (lower)-expressing cells compared to parental cells without endogenously tagged TET2. The number of peaks enriched in parental cells are also shown (inverse peak calling). (C) ChIP-qPCR for TET2 binding in ES cells using antibodies raised against endogenous TET2. Two positive regions (an intronic DNase I hypersensitivity site in Tet3 and an enhancer region in the Manba gene) as well as a negative control region are shown. Data are presented as mean enrichment over input with error bars depicting technical triplicates. The average fold enrichment over Tet2 knockout control cells is indicated.