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. Author manuscript; available in PMC: 2023 Mar 15.
Published in final edited form as: Nat Struct Mol Biol. 2022 Nov 11;29(11):1136–1144. doi: 10.1038/s41594-022-00855-y

Fig. 2 |. CTCF inhibits uasTrx directly and proximally, and independently of its architectural functions.

Fig. 2 |

a, Illustration of the experimental strategy and summarized findings from this figure and Extended Data Figs. 3–5. b, Genome browser views of CTCF ChIP-seq, PRO-seq and 4C-seq signals at Ahcyl1. Arrows indicate CTCF motif orientation. 4C-seq anchored at the Ahcyl1 promoter with (4 h auxin) and without (0 h auxin) CTCF degradation. The orange anchor indicates the 4C-seq viewpoint. Sites of interest are indicated below the track and are highlighted by dashed boxes. c, Genome browser tracks of CTCF ChIP-seq and PRO-seq and representative 4C-seq profiles of Ahcyl1 control and edited clones. Similar observations were made in two or three independent 4C-seq experiments. The orange anchor indicates the 4C-seq viewpoint. Arrows indicate CTCF motif orientation. Scissors indicate CRISPR/Cas9-edited regions. d, RT–qPCR of Ahcyl1 uasTrx and sense transcription in control and edited clones. Transcripts were normalized to Gapdh (error bar indicates s.e.m.; n = 4, except for uasTrx control, proximal and distal CBS deletion rep1, for which n = 3). Same analyses with different primer pairs are depicted in Extended Data Fig. 4b,c.