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. 2022 Jan 20;11:e70878. doi: 10.7554/eLife.70878

Figure 3. Effects of spacing alterations resulting from natural genetic variation across mouse strains.

(A) Spacing distributions of PU.1 and C/EBPβ binding sites at co-binding sites. (B) Density plots showing the relationship between transcription factor (TF) binding activity and motif spacing for the co-binding sites. Log2 chromatin immunoprecipitation sequencing (ChIP-seq) tags were calculated within 300 bp to quantify the binding activity of PU.1 and C/EBPβ. The color gradients represent the number of sites. Spearman’s correlation coefficients together with p-values are displayed. (C, E, G) Absolute log2 fold changes of ChIP-seq tags between C57 and another strain for (C) PU.1 binding, (E) C/EBPβ binding, or (G) nascent transcripts measured by GRO-seq. Boxplots show the median and quartiles of every distribution. Cohen’s d effect sizes comparing against variant-free regions are displayed on top. (D, F, H) Correlations between change of spacing or position weight matrix (PWM) score and change of (D) PU.1 binding, (F) C/EBPβ binding, or (H) nascent transcript level. Spearman’s correlation coefficients together with p-values are displayed.

Figure 3—source data 1. Tag fold changes at individual sites for PU.1 chromatin immunoprecipitation sequencing (ChIP-seq).
Figure 3—source data 2. Tag fold changes at individual sites for C/EBPβ chromatin immunoprecipitation sequencing (ChIP-seq).
Figure 3—source data 3. Tag fold changes at individual sites for GRO-seq.
Figure 3—source data 4. Tag fold changes at individual sites for H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq).

Figure 3.

Figure 3—figure supplement 1. Size distributions of insertions and deletions (InDels) at PU.1 and C/EBPβ co-binding sites across mouse strains.

Figure 3—figure supplement 1.

Figure 3—figure supplement 2. Functional motifs identified by MAGGIE for different transcription factor (TF) binding.

Figure 3—figure supplement 2.

Figure 3—figure supplement 3. Absolute log2 fold changes of chromatin immunoprecipitation sequencing (ChIP-seq) tags in relationship with the initial spacing between PU.1 and C/EBPβ motif in the reference mm10 genome.

Figure 3—figure supplement 3.

Solid lines represent means based on all four pairwise comparisons.
Figure 3—figure supplement 4. Absolute log2 fold changes of C/EBPβ chromatin immunoprecipitation sequencing (ChIP-seq) tags between C57 and another strain separately showing the distributions of promoters (left) and enhancers (right).

Figure 3—figure supplement 4.

Supplementary to Figure 3E.
Figure 3—figure supplement 5. Spacing distributions between lineage-determining transcription factors (LDTFs) and signal-dependent transcription factors (SDTFs).

Figure 3—figure supplement 5.

Left: p65 and PU.1. Right: p65 and c-Jun.
Figure 3—figure supplement 6. Absolute log2 fold changes of chromatin immunoprecipitation sequencing (ChIP-seq) tags between C57 and another strain for lineage-determining transcription factors (LDTFs) and signal-dependent transcription factors (SDTFs).

Figure 3—figure supplement 6.

(A) PU.1 and p65 binding at their co-binding sites and (B) c-Jun and p65 binding at their co-binding sites.
Figure 3—figure supplement 7. Correlations between changes in transcription factor (TF) binding activity and changes in (A) nascent transcription measured by GRO-seq or (B) the H3K27ac level measured by chromatin immunoprecipitation sequencing (ChIP-seq).

Figure 3—figure supplement 7.

Spearman’s correlation coefficients together with p-values are displayed.
Figure 3—figure supplement 8. Effects of genetic variation on H3K27ac level.

Figure 3—figure supplement 8.

(A) Absolute log2 fold changes of H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq) tags between C57 and another strain. (B) Correlations between change of spacing or position weight matrix (PWM) score and change of H3K27ac level. Spearman’s correlation coefficients together with p-values are displayed.