Fig. 7: Chromatin accessibility at the ZFP266 target loci affects reprogramming efficiency. | Nature Communications

Fig. 7: Chromatin accessibility at the ZFP266 target loci affects reprogramming efficiency.

From: B1 SINE-binding ZFP266 impedes mouse iPSC generation through suppression of chromatin opening mediated by reprogramming factors

Fig. 7

A Day 9 and day 14 after OSKM induction with overexpression of either BFP, VPR only or VPR-Zfp266. Red; mOrange, Green; Nanog-GFP. B Quantification of Nanog-GFP+ colony numbers at day 9 and day 14. Data represents an average of three independent experiments. Error bars indicate SEM. p-values calculated using a one-way ANOVA test. C Mechanistic model depicting how Zfp266 KO enhances reprogramming. Source data are provided as a Source Data file. B1 SINEs are strongly associated with nucleosomes and often have KLF and SOX motif at the head and tail due to G and A rich sequence, respectively. ZFP266 binds to some of SINEs in a cell type- and context-dependent manner. Upon reprogramming factor expression, ZFP266 is recruited to B1 SINE with KLF/SOX motifs at its head or tail, respectively, and impedes chromatin opening (top). Zfp266 KO results in increased chromatin accessibility in those loci, facilitating pluripotency gene expression.

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