Supplemental Material for Baker et al., 2018

<p><b>Table S1</b>. Summary of sequencing libraries..</p> <p><b>Table S2. </b>Biparental peakome for male germ cells showing the genomic coordinates of each peak in both the reference (mm10) and DBA/2J assembly.</p> <p><b>Table S3. </b>Mapping results for each H3K4me3 interval in the peakome and annotations.</p> <p><b>Table S4. </b>Summary of WGCNA modules.</p> <p><b>Table S5. </b>Summary of cis/trans test for BXD75 and BXD87 in hepatocytes, cardiomyocytes, and mESCs.</p> <p><b>Table S6</b>. Transcription factor motifs enriched in module H3K4me3 peaks.</p> <b>Table S7. </b>De novo genetic map for BXD strains.<div><b>Figure S1</b>. De novo genotypes from ChIP-seq data correct inconsistency between genotype and H3K4me3 phenotypes. <br><div><b>Figure S2</b>. Genotyping by ChIP-seq allows for hotspot level resolution for genetic mapping. <br></div></div><div><b>Figure S3. </b>Pearson Correlations for all hepatocytes, cardiomyocytes, and ESCs. <br></div><div><b>Figure S4. </b>The<b> </b>Chr 13 QTL is genetically compound.<br></div><div><b>Figure S5. </b>Functional annotation of H3K4me3 peaks.<br></div><div><b>Figure S6. </b>Hierarchical clustering based on H3K4me3 levels for all Parental, F1, and BXD lines.<br></div><div><br></div>