TET2 binding to enhancers facilitates transcription factor recruitment in hematopoietic cells

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Figure 1.
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.

This Article

  1. Genome Res. 29: 564-575

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