Fig. 2

ZNF676 and ZNF728 target respectively LTR12 and ERV9 elements and are able to repress their TE targets through the recruitment of KAP1. A Heatmap displaying KAP1, NFYA/B ChIP-seq & KZFP ChIP-exo enrichment over LTR12/ERV9 family members. KZFP ChIP-exo in HEK293T. NFYA/B ChIP-seq in K562 cells from ENCODE. KAP1 ChIP-seq in naive hESCs from [79]. p-value obtained by binomial test, corrected for TE subfamily size. B ZNF676 and ZNF728 averaged expression across embryonic development, RNA-seq from [88]. Error bars represent biological replicates. C ZNF676 and ZNF728 expression in reset to naive and primed WIBR3 hESCs, RNA-seq from [80]. D Multiple sequence alignments of LTR12C loci and 3 ERV9 subfamilies (gaps = grey, aligned sequences = white) overlaid with ZNF676-HA and ZNF728-HA in HEK293T cells and KAP1 in naive hESC ChIP-seq signals (colored). Proviral genomic features of ERV9 elements as detected by RetroTector, features of LTR12C as described in [49]. E HA immunoprecipitation of stably expressed ZNF676-HA and ZNF728-HA in K562 cells, followed by western blot detection of KAP1. F GFP fluorescence intensity across time in repression assay experiments (biological replicates, n=2). TE loci cloned upstream of PGK-GFP cassette are co-transduced with ZNF676, ZNF728 or LacZ with subsequent doxycycline-mediated induction at d0. G Dot plot representing (in red) ZNF676 and KAP1 targets among genes deregulated upon ZNF676 shRNA-mediated knockdown in Win1 naive embryonic stem cells