Fig. 4. Mechanism and genome-wide significance of the Nanog/Tet1 interaction.

a, Scatterplot showing the observed vs. expected overlap in genomic binding sites of Nanog and Tet1 according to comparisons performed in Supplementary Table 3. b, Ranked list of common targets of Nanog and Tet1 based on the comparisons in Supplementary Table 3. c, Schematic representation of ES cells harboring a doxycycline (Dox)-suppressible Nanog transgene in a Nanog^−/− genetic background²¹. d, Western blot analysis of Oct4, Nanog, and Tet1 expression in NgcKO ES cells treated with (+) or without (-) Dox. e, Overlapping peaks of Tet1 and Nanog from ChIP-Seq studies^16–18 in the Esrrb locus. f, Relative enrichment of Tet1 in the absence (−) and presence (+) of Dox in the Esrrb genomic locus as shown in (e). g, Transcriptional priming of Esrrb and Oct4 by Nanog and Tet1 in reprogramming intermediates. h, Relative enrichment of 5hmC and 5mC in the Esrrb and Oct4 loci. Error bars indicate standard deviation (n=3).